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Immune System OVERVIEW. Function major defense against infectious organisms
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1. THE IMMUNE SYSTEM Care of Clients with Altered Immunity
2. Immune System OVERVIEW Function major defense against infectious organisms & abnormal or damaged cells
Defends against bacteria, viruses, fungi & parasites
Removes & destroys damaged/dead cells
Identifies & destroys malignant cells
Self versus Non self. This is what immunity is all about. It is the ability of the cells of the body to be able to recognize cells or things that are not part or the normal body. How does the immune system know what is self? Each of us has specific cell surface characteristics which dont perfectly match anyone else. Exception is identical twins. This is called our Human Leukocytic Antigens or HLAs Auto-immune problems occur when the body doesnt recognize self & attacks it. Organ transplants are rejected because the donated organ has a different HLA than the host & the hosts immune system doesnt recognize the HLA & attacks & destroys the transplant. Functions of the immune system are: (1)defense against bacteria, viruses, fungi and parasites. (2) homeostasis by removing and destroying damaged cells, and (3) surveillance by identifying continuous malignant cells and destroying them.Self versus Non self. This is what immunity is all about. It is the ability of the cells of the body to be able to recognize cells or things that are not part or the normal body. How does the immune system know what is self? Each of us has specific cell surface characteristics which dont perfectly match anyone else. Exception is identical twins. This is called our Human Leukocytic Antigens or HLAs Auto-immune problems occur when the body doesnt recognize self & attacks it. Organ transplants are rejected because the donated organ has a different HLA than the host & the hosts immune system doesnt recognize the HLA & attacks & destroys the transplant. Functions of the immune system are: (1)defense against bacteria, viruses, fungi and parasites. (2) homeostasis by removing and destroying damaged cells, and (3) surveillance by identifying continuous malignant cells and destroying them.
3. Types of immunity Innate (natural) present at birth
Occurs without prior contact with antigen. Involves neutrophils & monocytes Immunity is classified as innate or acquired. Innate immunity (natural immunity) is present at birth and exists in a person without prior contact w3ith an antigen.Immunity is classified as innate or acquired. Innate immunity (natural immunity) is present at birth and exists in a person without prior contact w3ith an antigen.
4. Types of Immunity - Acquired Active (natural) development of antibodies & sensitized lymphocytes following exposure to disease. (measles, chickenpox, mumps)
Active (artificial) development of antibodies after injection of antigen (immunizations)
Takes time to develop long lasting Acquired immunity is calssifed as (1) active or natural which occurs following exposure to a disease such as measles, chickenpox or mumps; (2) active or artificial which orrucs as the result of an injection of an antigen such as immunizations. These types take time to develop but last a long time..Acquired immunity is calssifed as (1) active or natural which occurs following exposure to a disease such as measles, chickenpox or mumps; (2) active or artificial which orrucs as the result of an injection of an antigen such as immunizations. These types take time to develop but last a long time..
5. Types of Immunity - Passive Natural antibodies to antigen given to host rather than having to synthesize them (mother to fetus)
Artificial short-term. immediate immunity through injection of gamma-globulin (GG to protect against Hep B)
No memory cells so short lived Acquired psssive immunity can oruc naturally as the ressult of antiboides being passed from mother to fetus or may be adquired artificially through injection of jamma-globulin (GG) to produce short term protction from disease. These types are short lived because no memory cells are present.Acquired psssive immunity can oruc naturally as the ressult of antiboides being passed from mother to fetus or may be adquired artificially through injection of jamma-globulin (GG) to produce short term protction from disease. These types are short lived because no memory cells are present.
6. Review of Immunity Please review anatomy and physiology of the immune system and notes from Fundamentals.
Watch VT 137 and VT 134
7. Types of Immune Response Humoral Immunity (antibody-mediated)
B cells divide & differentiate into plasma cells after antigen invades
Plasma cells product & secrete antigen-specific immunoglobulins (Ig)
There are two types of immune responses. They are humoral or plasma mediated and cell-mediated. In humoral immunity, an invading antigen causesthe B cells to divide and diffenentiate into plasma cells which secrete antigen-specific immunoglobulins ( Ig)There are two types of immune responses. They are humoral or plasma mediated and cell-mediated. In humoral immunity, an invading antigen causesthe B cells to divide and diffenentiate into plasma cells which secrete antigen-specific immunoglobulins ( Ig)
8. Five types of Ig IgA, IgG and IgM respond to viral and bacterial invasion.
IgD may assist in B cell binding with antigen
IgE is present during inflammatory responses and causes allergic response
There are five types of Ig. IgA, IgG and IgM respond to viral and bacterial invasion. IgD may asist in B cell binding with the antigen. IgE is present during inflammatory responses and causes allergic reactions..There are five types of Ig. IgA, IgG and IgM respond to viral and bacterial invasion. IgD may asist in B cell binding with the antigen. IgE is present during inflammatory responses and causes allergic reactions..
9. Complement Consists of approx 25 enzymes that work with antibodies to help with puncturing bacterial cell walls to destroy (during humoral response) During the humoral response, complement which consists of approximately 25 enzymes, works with antibodies to puncture the bacterial cell walls to destroy them.During the humoral response, complement which consists of approximately 25 enzymes, works with antibodies to puncture the bacterial cell walls to destroy them.
10. Types of Immune Response Cell-Mediated occurs when antigen lives within the body cell (bacteria, virus, fungus, cancer)
Macrophages identify antigen & T cells (killer Ts, cytoxic cells) & defend against it.
Delayed response- graft rejection, hypersensitivity reactions, tumor immunity, immunity against bacteria, virus & fungus
Antigen specific Antigen must be present on cell surface In cell-mediated immunity,the antigensuch as bacteria, virus, fungus or cancer, lives within the body cell and is present on the cell surface. Macrophages indentify the antigen and T cell defend against it. This is a delayed response such as might orrur in graft rejection, hypersensitivy reactions, tumor immunity and immunity against bacteria, virus and fungus.In cell-mediated immunity,the antigensuch as bacteria, virus, fungus or cancer, lives within the body cell and is present on the cell surface. Macrophages indentify the antigen and T cell defend against it. This is a delayed response such as might orrur in graft rejection, hypersensitivy reactions, tumor immunity and immunity against bacteria, virus and fungus.
11. ALTERED IMMUNE RESPONSES Immunoincompetance
Severe infection, immunodeficiency diseases, malignancy
Overactive System
hypersensitivities
Immunocompetence exists when the immune system is able to identify and destroy foreign susstances. When the immund system in not competent to recognise or sestroy foreing susbtanves, infecton, immunofeficiency diseases and cancer orruc. When the immune system is overactive, hypersensitivies such as allergies and autoimmune diseases occur.Immunocompetence exists when the immune system is able to identify and destroy foreign susstances. When the immund system in not competent to recognise or sestroy foreing susbtanves, infecton, immunofeficiency diseases and cancer orruc. When the immune system is overactive, hypersensitivies such as allergies and autoimmune diseases occur.
12. TYPES OF HYPERSENSITIVIIES Type 1 anaphylactic local
IgE antibodies produced after 1st exposure
2nd exposure causes smooth muscle contraction, increased vascular permeability, vasodilation, hypotension, increased mucous & itching d/t IgE causing release of chemical mediators
There are four types of hypersensitivities, Type 1 is known as an anaphylactic reaction. On the first exposure to the allergen, IgE antibodies are produced and bind to mast cells and basophils. On next exposure, the allergen ataches to the IgE bound to mast cells or basopjils and causes release of chemical mediators from the cells. These chemicals cause vasodialation, dypotension, increased secretion of mucus, and itching.. Acutanous response , a sheal-and-flare ration orrucs. An example is a mosquito bite. Examples or the cause for local anaphylaxis is fool, pollen, medication and dust. There are four types of hypersensitivities, Type 1 is known as an anaphylactic reaction. On the first exposure to the allergen, IgE antibodies are produced and bind to mast cells and basophils. On next exposure, the allergen ataches to the IgE bound to mast cells or basopjils and causes release of chemical mediators from the cells. These chemicals cause vasodialation, dypotension, increased secretion of mucus, and itching.. Acutanous response , a sheal-and-flare ration orrucs. An example is a mosquito bite. Examples or the cause for local anaphylaxis is fool, pollen, medication and dust.
13. ANAPHYLATIC REACTIONS Local response is cutaneous (wheal-and-flare). Example of cause food, pollen, Rx, dust
Systemic response is anaphylaxis
shock, rapid, weak pulse, hypotension, dyspnea, bronchial edema, crackles, wheezing, laryngeal edema, angioedema, increased mucous, strider &death if not treated STAT.
Examples of cause food (shellfish, nuts peanuts, eggs, strawberries), Rx (PCN, Sulfas) insect bites (bees wasps), antitoxin, (tetanus, rabies) blood, iodine-contrast media for IVP
Anaphylaxis occurs when the chemical mediators are released systemically. Anaphylaxis may be caused by food, particularly, shellfisk, nuts, eggs and strawberries, drugs like PCN and Sulfa, insect bites (bees an d wasps)antitoxins like Rabies or tetanum, and iodine-contrast media for IVPs and MRIs. Anaphylaxis can orrrur rapidly and is a medical emergency. Symptoms of anaphylactic shock include rapid, weak pul;se, hypotension, dyspnea, bronchiual edema, crackles, wheezing, laryngeal edama, angioedema, increased mucous, stider and death if not treated immediately. Anaphylaxis occurs when the chemical mediators are released systemically. Anaphylaxis may be caused by food, particularly, shellfisk, nuts, eggs and strawberries, drugs like PCN and Sulfa, insect bites (bees an d wasps)antitoxins like Rabies or tetanum, and iodine-contrast media for IVPs and MRIs. Anaphylaxis can orrrur rapidly and is a medical emergency. Symptoms of anaphylactic shock include rapid, weak pul;se, hypotension, dyspnea, bronchiual edema, crackles, wheezing, laryngeal edama, angioedema, increased mucous, stider and death if not treated immediately.
14. Anaphylactic Shock Treatment:
ABCs must be established.
Epinephrine 1:1000, 0.2 to 0.5ml SQ STAT or IV if severe
(causes vasoconstriction and bronchodilation)
Benadryl IM or IV
Histamine H2 blockers (Tagamet) Treatment for shock must be initiated STAT. Respiratory and cardiovascular systems must be assessed and monitored. Epinephrine 1:1000, 0.2 to 0.5 ml should be giveneither SQ or IV if severe to causes vasoconstriction and bronchodilation. Benadryl IM or IV and Histamine H2 blockers such as Tagamet to decrease angioedema and urticariaTreatment for shock must be initiated STAT. Respiratory and cardiovascular systems must be assessed and monitored. Epinephrine 1:1000, 0.2 to 0.5 ml should be giveneither SQ or IV if severe to causes vasoconstriction and bronchodilation. Benadryl IM or IV and Histamine H2 blockers such as Tagamet to decrease angioedema and urticaria
15. Treatment cotinued Oxygen is used to maintain O2 sat above 90%.
HOB 45 degrees to assist with respiratory status.
Maintain BP (fluids, vasopressors dopamine & norepinephrine)
Aminophylline IV 6 mg/kg for severe bronchospasm.
Albuterol nebs Q2 - 4 hrs
Corticosteroids Oxygen is given to maintain O2 sat at above 90%. The head of the bed should be raised to 45 degrees to assist with resssssssssssssssssssssssssssspiration. Blood pressure should be maintained with fluids and vasopressors such as dopamine and norepinephrine. Amionophylline is given IV at 6 mg/kg for severe bronchospasns. Albuterol nebs may be given every 2 4 hours. Oxygen is given to maintain O2 sat at above 90%. The head of the bed should be raised to 45 degrees to assist with resssssssssssssssssssssssssssspiration. Blood pressure should be maintained with fluids and vasopressors such as dopamine and norepinephrine. Amionophylline is given IV at 6 mg/kg for severe bronchospasns. Albuterol nebs may be given every 2 4 hours.
16. Treatment continued Monitor VS,O2 sat, LOC, cardiac & respiratory status.
Anticipate CPR, intubation & tracheotomy Vital signs, O2 sat, level of consconcious, cardiac and respiratory status should continue to be monitored and the RN should anticipate CPR, intubation and tracheotomy if necessary.Vital signs, O2 sat, level of consconcious, cardiac and respiratory status should continue to be monitored and the RN should anticipate CPR, intubation and tracheotomy if necessary.
17. ANAPHYLACTIC REACTIONS Atopic reactions
Allergic rhinitis (hay fever)
Asthma bronchial constriction, excessive mucous, mucous membrane edema, dyspnea, wheezing, coughing, tight chest Other examples of anaphylactic reactions are called Atopic reactions. These include allergic ghinitis, commonly known as hay fever, brobnchial asthma, atopic dermatitis, urticaria, and angioedema. Individuals who experience these disorders have inherited an increased tendancy to be sensitive to the environmental allergens. Hay fever is the most common. Symptoms are runny nose and eyes, sneezing, mucosal swelling and puritus around the eyes, nose, throat nad mouth. Symptoms of asthma are listed on this slide.Other examples of anaphylactic reactions are called Atopic reactions. These include allergic ghinitis, commonly known as hay fever, brobnchial asthma, atopic dermatitis, urticaria, and angioedema. Individuals who experience these disorders have inherited an increased tendancy to be sensitive to the environmental allergens. Hay fever is the most common. Symptoms are runny nose and eyes, sneezing, mucosal swelling and puritus around the eyes, nose, throat nad mouth. Symptoms of asthma are listed on this slide.
18. ANAPHYLACTIC REACTIONS Atopic reactions continued
atopic dermatitis chronic, inherited disorder involving reddened vesicles, crust & cracks
Urticaria (hives)
Angioedema edema of face,, hands & feet, larynx, GI tract & genitalia. Atopic dermatitisinvolves generalized skin lesions which are vesicular and edematous. Urticaria or hives develops rapidly after exposure to an allergen and lasts for minutes to hours. Hives represents a wheal-flare response to the allergen. Angiledema is a localized skin reactionsimiliar to hives beeeeeeeebut involving deeped layers of skin and submucosa. Swelling is usually seen in the eyelids, lips, tonjue, larunz, hands, feet, GI tackt and genitalia. This can be a medical emergency if respiration is compromised. Atopic dermatitisinvolves generalized skin lesions which are vesicular and edematous. Urticaria or hives develops rapidly after exposure to an allergen and lasts for minutes to hours. Hives represents a wheal-flare response to the allergen. Angiledema is a localized skin reactionsimiliar to hives beeeeeeeebut involving deeped layers of skin and submucosa. Swelling is usually seen in the eyelids, lips, tonjue, larunz, hands, feet, GI tackt and genitalia. This can be a medical emergency if respiration is compromised.
19. Type II IgM & IgG produce a cytotoxic reaction that destroys the target cell.
Cause exogenous (foreign tissue, blood incompatibility, drug)
Or endogenous (autoimmune disorders autoimmune hemolytic anemia,Goodpastures syndrome) Type II hpypersentitiv reactions are cytotoxic and cytolytic and destroy cells by binding IgM and IgE to cell surfaces which activates complement and phagocytosis. /examples of Type II reactions are blood transfusion reactions because of blood incompatibility, and drug- related hemolytic anemias. Goodpasture sysdrome is a rare disease in which the lungs and kisneys are damaged due to endogenous antibodies interacting with tissue andigens. Pulmonary hemmorrhage and glomerulonephritis result.
Type II hpypersentitiv reactions are cytotoxic and cytolytic and destroy cells by binding IgM and IgE to cell surfaces which activates complement and phagocytosis. /examples of Type II reactions are blood transfusion reactions because of blood incompatibility, and drug- related hemolytic anemias. Goodpasture sysdrome is a rare disease in which the lungs and kisneys are damaged due to endogenous antibodies interacting with tissue andigens. Pulmonary hemmorrhage and glomerulonephritis result.
20. Type III Immune complex - mediated reactions. IgG & IgM
Produces complexes which are then deposited in small blood vessel walls. Sites include kidneys, skin, joints, and other small blood vessels. The deposited complexes activate complement, & tissue or vessel damage results
Rheumatoid arthritis and systemic lupus erythematosus IgG and IgM form immune compleXes in the body that get deposited in Vessel walls and extravascular tissues. Complement is activated and chemical mediatros of inflammation like histamine are released. Neutrophols respond to the inflammation that is created by the immune complexes increasing tissue damage. Streptococcla infections are also causes of Type III reactions.
Serum sickness caused by foreing serums like horse serum for antitetanus. Penciillins and sulfonamides can cause serum sickness. Serum sickness produces fever, aarthritis, kuticaria and enlarged slpeen and lymh nodes 7 to 14 days after exposure . Treated with adrenal cortical hormones- gllucocortiocords and mineralcorticoids- these medications decrease the inflammatory process. IgG and IgM form immune compleXes in the body that get deposited in Vessel walls and extravascular tissues. Complement is activated and chemical mediatros of inflammation like histamine are released. Neutrophols respond to the inflammation that is created by the immune complexes increasing tissue damage. Streptococcla infections are also causes of Type III reactions.
Serum sickness caused by foreing serums like horse serum for antitetanus. Penciillins and sulfonamides can cause serum sickness. Serum sickness produces fever, aarthritis, kuticaria and enlarged slpeen and lymh nodes 7 to 14 days after exposure . Treated with adrenal cortical hormones- gllucocortiocords and mineralcorticoids- these medications decrease the inflammatory process.
21. Type IV Delayed hypersensitivity reactions
If a patient had previous exposure to TB, they will get a positive PPD. At the PPD injection site, T cells ( cell mediated) accumulate, release lymphokines, and recruit and activate macrophages. Induration and erythema occur 24 to 48 hours after exposure.
Contact dermatitis, poison ivy, TB, and graft reactions.
A Type IV reaction is a cell-mediated response, causing tissue damage. The response takes 24 to 48 hours to occur. It is characterized by an interaction between antigens and antigen-responsive T lymphocytes. Examples are cobtactk termatitis, poison ivy, PPD and transplant rejection.
A Type IV reaction is a cell-mediated response, causing tissue damage. The response takes 24 to 48 hours to occur. It is characterized by an interaction between antigens and antigen-responsive T lymphocytes. Examples are cobtactk termatitis, poison ivy, PPD and transplant rejection.
22. General Treatment for Allergic Reactions Remove allergen
Antihistamines
Decongestants
Corticosteroids
Antipruritics
Mast cell-stabilizing drugs After the cause of the allergic response has been identified, the client should avoid the allergen. This may simply involve avoiding certain foods< BUT MAY REQUIRE THAT HE MAKE MAJOR LIFE CHANGES SUCH AS CHANGING OCCUPATIONS, MOVING TO A DIFFERENT CLIMATE OR GIVING UP A Pet. If a drug is the cause, he should avoid it and wear an Medic Alert bracelet, identifying the allergy. Drug therapy includes antihistimines for allergic rhinitis and urticaria. They work by blocking the histamine receptor sites. Sympathomimetic/decongestant drugs include Epinephrine (Adrenalin) as the treatment of choice for anaphylactic reactions. Minor decongestants include NeoSynephrine and Sudafed to treat allerfgic rhinitis. Corticosteroid nose sprays are effective for allergic rhinitis and oral corticosteroids are given for more severe allergic reactions. Antipruritics include topicals - calamine lotion, coal tar solutions, menthol and camphor. Mast cell-stabilizing drugs are used to asthma and allergic rhinitis. Examples are Cromolyn (Nasalcrom) and nedocromil (Tilade). They block release of histamines, leukotrienes and other chemicals from the mast cell after antigen- IgE interaction. After the cause of the allergic response has been identified, the client should avoid the allergen. This may simply involve avoiding certain foods< BUT MAY REQUIRE THAT HE MAKE MAJOR LIFE CHANGES SUCH AS CHANGING OCCUPATIONS, MOVING TO A DIFFERENT CLIMATE OR GIVING UP A Pet. If a drug is the cause, he should avoid it and wear an Medic Alert bracelet, identifying the allergy. Drug therapy includes antihistimines for allergic rhinitis and urticaria. They work by blocking the histamine receptor sites. Sympathomimetic/decongestant drugs include Epinephrine (Adrenalin) as the treatment of choice for anaphylactic reactions. Minor decongestants include NeoSynephrine and Sudafed to treat allerfgic rhinitis. Corticosteroid nose sprays are effective for allergic rhinitis and oral corticosteroids are given for more severe allergic reactions. Antipruritics include topicals - calamine lotion, coal tar solutions, menthol and camphor. Mast cell-stabilizing drugs are used to asthma and allergic rhinitis. Examples are Cromolyn (Nasalcrom) and nedocromil (Tilade). They block release of histamines, leukotrienes and other chemicals from the mast cell after antigen- IgE interaction.
23. Assessing the Immune System Age-Related Changes Decreased size & activity of thymus
Decreased production of T and B cells
Delayed hypersensitivity response.
Decreased cell-mediated immunity
Greater susceptibility to infection
Higher incidence of tumors
. Encourage older adult to eat well-balanced diet, drink adeq fluids, get flu & pneumonia shots. Practice good handwashing. Report fever or other signs of infection, changes in mental status, behavior or levels of activity
The elderly have a decline in the immune system. There are decreased size and activity of the thymus, decreased production of T and B cells, delayed hypersensitivity responses, decreased cell-mediated immunity,greater susceptibility to infection and higher incidence of tumors.Encourage older adult to eat well-balanced diet, drink adeq fluids, get flu & pneumonia shots. Practice good handwashing. Report fever or other signs of infection, changes in mental status, behavior or levels of activity
The elderly have a decline in the immune system. There are decreased size and activity of the thymus, decreased production of T and B cells, delayed hypersensitivity responses, decreased cell-mediated immunity,greater susceptibility to infection and higher incidence of tumors.
24. Assessing the Immune System Weight changes, skin lesion, rashes, or impaired healing.
Activity intolerance, frequent sore throats, URI, swollen glands, easy brusing, joint pain, swelling, enlarged lymph nodes.
Acute: erythema, local heat, pain, T > 100.4, P >90, R > 20, The sysptoms listed above may indicated an problem with immunity.The sysptoms listed above may indicated an problem with immunity.
25. Assessment chronic allergy Skin rashes, itching
EENT conjunctivitis, dark circles under eyes, excessive rubbing/ blinking, recurrent ear infection, diminished hearing, nasal voice rhinitis, pale, swollen mucous membranes, throat clearing, swollen lips/ tongue, enlarged lymph nodes These sypmtoms are indicative of chronic allergies.These sypmtoms are indicative of chronic allergies.
26. Diagnostic Studies Lymphocyte count below 12/ml in cellular immunodeficiency.
Eosinophil count elevated in type 1 hypersensitivity
Radioallergosorbent test (RAST) confirms allergy to specific food or drugs
Skin testing determines hypersensitivity to allergens RAST test measures the quantity of antigen-specific Ig E in the blood. Is less sensitive and more expensive than skin test has no risk of anaphalaxis. Skin tests involves pricking the skin with suspected allergans or intrjecting indrdermally. A local wheal-and-flare response indicates an allergy to the allergen. A very sensitive person is at risk for having an anaphylactic reaction.
Diagnostic tests used to confirm immunodeficiency problems include a CBC with WBC diffenential including an absolute tymphocyte and eosinophil count. Cellular immunodeficiency ios diagnosed if the lymphocyte count is below 122/microliters. The eosinophil count is elevated with type I hypersensitivity reactions involving IgERAST test measures the quantity of antigen-specific Ig E in the blood. Is less sensitive and more expensive than skin test has no risk of anaphalaxis. Skin tests involves pricking the skin with suspected allergans or intrjecting indrdermally. A local wheal-and-flare response indicates an allergy to the allergen. A very sensitive person is at risk for having an anaphylactic reaction.
Diagnostic tests used to confirm immunodeficiency problems include a CBC with WBC diffenential including an absolute tymphocyte and eosinophil count. Cellular immunodeficiency ios diagnosed if the lymphocyte count is below 122/microliters. The eosinophil count is elevated with type I hypersensitivity reactions involving IgE
27. Histocompatibility HLA Typing
Crossmatching HLA is done to determine if it matches the HLA of the doner prior to Histocompatibility is essential prior to matching donors and recepients or blood, bone marrow and organ transplants. The human leukocyte antigen system is a series of inherited genes that occur on the sixth chromosome in humans. Typing of ones transplant. Antigen matches of 5 6 antigens results in less likely rejection of the tissue. Crossmatching mixes blood from the doner and potential recepient to determine any cytotoxic (anti-HLA) antibodies to the doner blood. A negative crossmatch indicated no cytotoxic antibodies are present and transplant should have a positive outcome. HLA is done to determine if it matches the HLA of the doner prior to Histocompatibility is essential prior to matching donors and recepients or blood, bone marrow and organ transplants. The human leukocyte antigen system is a series of inherited genes that occur on the sixth chromosome in humans. Typing of ones transplant. Antigen matches of 5 6 antigens results in less likely rejection of the tissue. Crossmatching mixes blood from the doner and potential recepient to determine any cytotoxic (anti-HLA) antibodies to the doner blood. A negative crossmatch indicated no cytotoxic antibodies are present and transplant should have a positive outcome.
28. IMMUNODEFICIENCY DISORDERS Occur when immune cells are improperly developed or absent
Example: Graft-versus-host disease occurring after transfusion or transplant with cells that dont match the recipient In most transplant situations, the concern is that the host will reject the graft, but in GVHD, the graft rejects the host. The new donor cells recognize the host as foreign and within 7 to 30 days, the donor T cells attack and destroy vulnerable host cells. GVHD targets the skin, GI tract and liver. Symptoms include a painful, itching rash that begins on the sold and palms and covers the chest, back and legs, causing desquamation. Liver involvement includes mild jaundice and elevated liver enzymes. GI symptoms include diarrhea, abdominal pain, bleeding and malabsorption. The biggest problem is infection bacterial, viral and fungal. GVHD is most often seen following bone marrow transpolant. In most transplant situations, the concern is that the host will reject the graft, but in GVHD, the graft rejects the host. The new donor cells recognize the host as foreign and within 7 to 30 days, the donor T cells attack and destroy vulnerable host cells. GVHD targets the skin, GI tract and liver. Symptoms include a painful, itching rash that begins on the sold and palms and covers the chest, back and legs, causing desquamation. Liver involvement includes mild jaundice and elevated liver enzymes. GI symptoms include diarrhea, abdominal pain, bleeding and malabsorption. The biggest problem is infection bacterial, viral and fungal. GVHD is most often seen following bone marrow transpolant.
29. GVHD TREATMENT There is no adequate treatment.
Drug therapy
Calcineurin inhibitors Prograf, Sandimmune
Antimetabolites - CellCept
Corticosteroids Solu-Medrol
Antibiotics, antivirals, antifungals Calcineurin inhibitors inhibit production of T cytoxic lymphocytes. Amtimetabolites suppress proliferation of T and B cells. Corticosteroids suppress inflammatory response and inhibit cytokine production and T cell activation. Typically, these three categories are used together. Please review side effects in your Pharmacology and Nursing textbooks. Infections are treated with antibiotics, antivirals or antifungals.Calcineurin inhibitors inhibit production of T cytoxic lymphocytes. Amtimetabolites suppress proliferation of T and B cells. Corticosteroids suppress inflammatory response and inhibit cytokine production and T cell activation. Typically, these three categories are used together. Please review side effects in your Pharmacology and Nursing textbooks. Infections are treated with antibiotics, antivirals or antifungals.
30. INTERVENTION RISK FOR INFECTION HANDWASHING
Reverse isolation
Monitor vital signs, assess for signs of infection, I/O, urine output
Have patient wear mask and gloves when out of room
Adequate hydration and nutrition
Oral hygiene Risk for infection is the biggest problem with GVHD. Careful handwashing for both cloient and the healthcare team is essential. Reverse isolation, adequate hydration and nutrition, and good oral hygiene are a must and careful monitoring for signs of infection and complications are required.Risk for infection is the biggest problem with GVHD. Careful handwashing for both cloient and the healthcare team is essential. Reverse isolation, adequate hydration and nutrition, and good oral hygiene are a must and careful monitoring for signs of infection and complications are required.
31. Risk for Impaired Tissue Integrity Assess for graft rejection if organ transplant
Erythemia. Swelling over site, fever, increased WBCs,
Monitor labs
Assess for graft versus host
Administer immunosuppressive therapy.
If the client has received an organ transplant, he should be continually asses for graft rejection. Sings of rejection include erythemia and swelling over the4 site, and eolevate4d temperature along with increased WBCs. This client should be assessed for GVHD and is treated with immunosuppressive therapy and should be monitored for infection.lIf the client has received an organ transplant, he should be continually asses for graft rejection. Sings of rejection include erythemia and swelling over the4 site, and eolevate4d temperature along with increased WBCs. This client should be assessed for GVHD and is treated with immunosuppressive therapy and should be monitored for infection.l
32. AUTOIMMUNITY Occurs when immune system can no longer recognize self from nonself
B and T cells attack self-antigen and cause physiologic tissue damage
Autoimmune disease depends on which self-antigen is involved
Most autoimmune diseases have genetic basis Autoimmune diseases are grouped according to organ-specific and systemic diseases. Several systemic diseases will be covered in this course. Organ-specific diseases will be covered in Advanced Adult Nursing and Pediatric NursingAutoimmune diseases are grouped according to organ-specific and systemic diseases. Several systemic diseases will be covered in this course. Organ-specific diseases will be covered in Advanced Adult Nursing and Pediatric Nursing
33. Connective Tissue Disorders Selected Systemic Autoimmune Disorders This section discusses selected systemic autoimmune disorders of the connective tissue.This section discusses selected systemic autoimmune disorders of the connective tissue.
34. Osteoarthritis (OA) Pathophysiology
progressive deterioration & loss of cartilage in joints
Cartilage becomes soft and yellow. Joint space narrows and osteophyte (bone spur) develops.
Articular surfaces erode because body cant repair cartilage as fast as it is destroyed.
Results in uneven stress on joint & decreased motion Osteoarthritis, also known as degenerative joint disease, involves a progressive deterioration and loss of cartilage in the joints. The cartilage becomes soft and yellow resulting in a narrowing of the space between joints. Bone spurs develop and there is uneven stress on the joints and decreased motion. Osteoarthritis, also known as degenerative joint disease, involves a progressive deterioration and loss of cartilage in the joints. The cartilage becomes soft and yellow resulting in a narrowing of the space between joints. Bone spurs develop and there is uneven stress on the joints and decreased motion.
35. OA Etiology:
Age, obesity, overuse of joint
Genetic factors, trauma, and joint sepsis. decreased estrogen
Signs and Symptoms:
joint pain with slight movement & at rest, enlarged joint, Heberdens nodes, Bouchards nodes, stiffness when at rest, loss of function of joint involved and decrease in ADLs. A single cause for OA has not been identified, but is is related to advancing age. Approximately 60% of clients over the age of 65 years have symptoms of the disease. After the age of 50, it is twice as great in females which suggests decreased estrogen as a cause. Obesity is related to OA of the knee. Strenous exercise and sports injuries have been linked to OA. Signs and symptoms include first, joint pain which gets worse with joint use. As OA progresses, joints become more painful, and enlarged. Heberdens and Bouchards nodes may be found on the fingers. If the spine is involved, the client may have difficulty sitting and rising from a chair. Knee involvments results in altered gait. Joint pain is increased with falling barometric pressure before rain. It is true that the client can predict rain in his bones.A single cause for OA has not been identified, but is is related to advancing age. Approximately 60% of clients over the age of 65 years have symptoms of the disease. After the age of 50, it is twice as great in females which suggests decreased estrogen as a cause. Obesity is related to OA of the knee. Strenous exercise and sports injuries have been linked to OA. Signs and symptoms include first, joint pain which gets worse with joint use. As OA progresses, joints become more painful, and enlarged. Heberdens and Bouchards nodes may be found on the fingers. If the spine is involved, the client may have difficulty sitting and rising from a chair. Knee involvments results in altered gait. Joint pain is increased with falling barometric pressure before rain. It is true that the client can predict rain in his bones.
36. OA Diagnostic
History, physical
No lab tests
ESR may be slightly elevated secondary to synovitis.
X-rays show structural joint changes.
CT, MRI, Bone scan show joint change
OA is diagnosed by history and physical. There are no lab tests, although the Sed rate may be elevatede is synovitis is present. Bone scan, CT and MRI may show early joint changes and xrays will show joint space narrowing.OA is diagnosed by history and physical. There are no lab tests, although the Sed rate may be elevatede is synovitis is present. Bone scan, CT and MRI may show early joint changes and xrays will show joint space narrowing.
37. Medications Pain Tylenol,NSAIDS,ASA
Capsaicin cream
Muscle Spasms Muscle Relaxants (Flexeril) The client with mild to moderate pain can use Tylenol and Capsaicin cream for relief. The cream should not be used with a heating pad. Other clients benefit from the NSAIThe client with mild to moderate pain can use Tylenol and Capsaicin cream for relief. The cream should not be used with a heating pad. Other clients benefit from the NSAI
38. Medications Pain Tylenol,NSAIDS,ASA
Capsaicin cream
Muscle Spasms Muscle Relaxants (Flexeril) The client with mild to moderate pain can use Tylenol and Capsaicin cream for relief. The cream should not be used with a heating pad. Other clients benefit from the NSAIDs or ASA. If the client experiences muscle spasms, an muscle relaxants such as Flexeril may be necessary. Review your Pharmacology notes for more information on these drugs.The client with mild to moderate pain can use Tylenol and Capsaicin cream for relief. The cream should not be used with a heating pad. Other clients benefit from the NSAIDs or ASA. If the client experiences muscle spasms, an muscle relaxants such as Flexeril may be necessary. Review your Pharmacology notes for more information on these drugs.
39. OA
Rest
Immobilization of joint
Positioning
Placed in functional position.
Large pillow under contracture (if present).
Elevate 8 to 12 inches.
Heat with
heating pads- max 20 min
The OA client needs to balance rest with activity. During acute pain, the joint should be rested and placed in a functional position, using pillows, splints, or braces. The joints should not be immobilized more than one week to prevent joint stiffness. Heat or cold applications may be helpful. Glucoosamine and chrondroitin sulfate may help with synthesis of new cartlage.The OA client needs to balance rest with activity. During acute pain, the joint should be rested and placed in a functional position, using pillows, splints, or braces. The joints should not be immobilized more than one week to prevent joint stiffness. Heat or cold applications may be helpful. Glucoosamine and chrondroitin sulfate may help with synthesis of new cartlage.
40. OA Diet
High protein, Vitamin C
Weight loss if indicated
Surgery Weight loss is very beneficial for OA of the knee in the obese client. A healthy diet should be followed for all OA clients. Surgery may be indicated for some clients.sWeight loss is very beneficial for OA of the knee in the obese client. A healthy diet should be followed for all OA clients. Surgery may be indicated for some clients.s
41. OA
Treatment options
Arthroscopy- visual inspection of joint
Ostotomy- incision into bone, can re-align bone. May help decrease pain.
Arthroplasty- reconstruction/replacement of joint. Can use screws or plates to hold joint in or cement joint.
Total joint replacement-hip/knee This slide lists some of the surgical treatment options.This slide lists some of the surgical treatment options.
42. Gout Genetic or secondary to conditions that increase uric acid. Urate crystals deposited into joints
Stress, Alcohol,some diuretics, cyclosporin and salicylates can induce
Acute Gouty Arthritis
Abrupt, acute pain, red, hot, swollen, tender joint
Chronic Tophaceous Gout
Tophi on joints, joint stiffness, limited ROM, deformity.
Hyperuricemia caused by increased uric aqcid production, underexcretion of uric acid by the kidneys of increase of foods containing purines (sardines, herring, muscles, liver, goose, sweetbreads). Stress, alcohol, thiazide diuretics, immunosuppressive drugs, and prolonged fasting can induce gout. Gouty arthritis usually affects no more than four joints, the most common being the great toe. The onset is rapid and it usually subsides in 2 to 10 days. Attacks can reoccur if not treated. Chronic gout involves multiple joints and tophi develop, causing deformityHyperuricemia caused by increased uric aqcid production, underexcretion of uric acid by the kidneys of increase of foods containing purines (sardines, herring, muscles, liver, goose, sweetbreads). Stress, alcohol, thiazide diuretics, immunosuppressive drugs, and prolonged fasting can induce gout. Gouty arthritis usually affects no more than four joints, the most common being the great toe. The onset is rapid and it usually subsides in 2 to 10 days. Attacks can reoccur if not treated. Chronic gout involves multiple joints and tophi develop, causing deformity
43. Diagnostic
Uric Acid level: above 7.5
WBC:
20,000, elevated Eosinophils
24 hours urine
Elevated uric acid
Arthrocentesis:
Synovial fluid aspirated, will see crystals
Treatment
Diet:
Increase fluids, avoid alcohol, red meats, organ meats
Monitor for kidney stones
Diagnosis can usually be made on clinical symptoms alone. Serum and urin uric acid levels will be elevated as will as WBCs Synovial fluid aspiration is usually not necessary. Treatment includes life style changes such as watching diet, losing weight if necessary and decreasing or avoiding alcohol. The client should be monitored for kidney stones. Rest of the joint, heat and cold applications may be helpfulDiagnosis can usually be made on clinical symptoms alone. Serum and urin uric acid levels will be elevated as will as WBCs Synovial fluid aspiration is usually not necessary. Treatment includes life style changes such as watching diet, losing weight if necessary and decreasing or avoiding alcohol. The client should be monitored for kidney stones. Rest of the joint, heat and cold applications may be helpful
44. Medications Allopurinol (Zyloprim)
Reduces uric acid.
Increase fluids, monitor kidneys.
NSAIDS & Steroids
To decrease inflammation- Indocin
Colchicine
Decreases urate crystals & inflammation.
Used to treat acute attacks and to prevent attacks.
Benemide for those who cant excrete uric acid.
Medications useful for treating gout are (1)Zyloprim which is useful during the acute stage and as a maintanence drug to prevent further attacks, (2) Colchicine used with NSAIDs and (3) Benemide which cant be used for clients who have reduced creatinine clearance. ASA must be avoided because it inactivates Banemid. Cozaar may be useful in promoting urate diuresis . Cozaar and Zyloprim may be given together. Medications useful for treating gout are (1)Zyloprim which is useful during the acute stage and as a maintanence drug to prevent further attacks, (2) Colchicine used with NSAIDs and (3) Benemide which cant be used for clients who have reduced creatinine clearance. ASA must be avoided because it inactivates Banemid. Cozaar may be useful in promoting urate diuresis . Cozaar and Zyloprim may be given together.
45. RHEUMATOID ARTHRITIS (RA) Chronic systemic disease characterized by inflammation of synovial joints
Periods of remission and exacerbation
Higher incidence between 40 and 60 years of age
Affects women 2 to 3 times more often than men
Smoking linked to RA RA is a chronic, systemiuc disease characterized by inflammation of connective tissue in the synovial joints. The cause is unknown but it is known to affect women between the age of 40 and 60 2-3 times more often than men. Smoking has also been linked to RA.RA is a chronic, systemiuc disease characterized by inflammation of connective tissue in the synovial joints. The cause is unknown but it is known to affect women between the age of 40 and 60 2-3 times more often than men. Smoking has also been linked to RA.
46. CAUSE Unknown, but autoimmunity and genetic theories accepted
Autoimmune theory abnormal IgG develops in response to an antigen
Autoantibodies (rheumatoid factor RF) develop against IgG
RF & IgG form immune complex & deposit in joints. Inflammation cause joint changes & later cartilage destruction by pannus The autoimmune and genetic theories explains that a genetically susceptible individual develops an abnormal IgG in response to a antigen and then develops autoantibodies known as rheumatoid factor (RF) against the abnormal IgG. These combine to form immune complexes and are deposited in the joints, causing inflammation and joint changes followed later by cartilage and destruction by a pannus.The autoimmune and genetic theories explains that a genetically susceptible individual develops an abnormal IgG in response to a antigen and then develops autoantibodies known as rheumatoid factor (RF) against the abnormal IgG. These combine to form immune complexes and are deposited in the joints, causing inflammation and joint changes followed later by cartilage and destruction by a pannus.
47. Rheumatoid Arthritis Pannus is vascular granulation tissue, composed of inflammatory cells, that erode cartilage, destroying bone. Fibrous adhesions, bony ankylosis, & calcifications occur, bone loses density and secondary osterporosis occurs.
. The pannus usually effects fingers, knees, and is worse in toes, ankles, and feet.
The pannus usually effects fingers, knees, and is worse in toes, ankles, and feet.