NUR 120 Week 6 Immune Disorders Infection Human Immunodeficiency Virus

NUR 120 Week 6 Immune Disorders Infection Human Immunodeficiency Virus
Genetics Altered Immune Responses and Transplantation

Nursing Care of Clients with Lymph Disorders
Bacterial, Viral, and Fungal Infections: Prevention, Assessment and Interventions. Infectious Diseases are leading cause of death worldwide. Previously controlled infections are re-emerging like malaria, tuberculosis, and pertussis. Newer infections have emerged over the last several decades including Lyme disease, Human Immunodeficiency virus (HIV), and Coronavirus (SARS)

Infectious Diseases in the US
The resistance of microorganisms produced a level of concern similar to infections in the pre-antibiotic era. Example: VRE, MRSA. Bioterrorism is the latest threat involving microorganism like smallpox, tularemia, plague and anthrax. Virulence – the ability of the pathogen (disease producing microorganism) to invade and injure the host (person).

Risk Factors for Infections
Environmental Excessive alcohol consumption →→ malnutrition Smoking Malnutrition Medication therapy (immunosuppressive agents) Glucocorticosteroid Cancer Chemotherapy Chronic Diseases DM Adrenal Insufficiency Renal Failure Hepatic Failure Chronic Lung Disease

Causes of Infections Bacteria
Micrograph of a bacteria colony forming. The bacterial colony is well developed, and is showing the initial development of a biofilm. Some of the round Cocci type bacteria are suspended in an adhesive matrix. Bacteria includes staphylococcus aureus, Escherichia Coli, Mycobacterium tuberculosis.

Virus AIDS Virus Virus are pathogenic organisms that use the host’s genetic machinery to reproduce ( HIV, Hepatitis, Herpes Simplex)

Fungus Fungus in the head Skin Fungus
Molds and yeast (Candida Albicans, Aspergillus)

Prions – Protein particles

Prions Prion is an infectious agent that is composed primarily of protein. To date, all such agents have been discovered to propagate by transmitting a misfolded protein state; as with viruses the protein itself does not self-replicate, rather it induces existing polypeptides in the host organism to take on the rogue form. The misfolded form of the prion protein has been implicated in a number of diseases in a variety of mammals, including bovine spongiform encephalopathy (BSE, also known as "mad cow disease") in cattle and Creutzfeldt–Jakob disease (CJD) in humans. All known prion diseases affect the structure of the brain or other neural tissue.

Parasites – Protozoa/Helminths
Protozoa – Malaria, Toxoplasmosis Helminths – Worms , flukes

Chain of Infection ↑ →→→→→→→Causative Agents→→→↓ ↑ ↓ ↑ Cycle of Infection Reservoir ↑ Portal of exit Susceptible Host from the host ↑ ↓ Port of entry to the host ←←←Mode of transmission

Diagnostic Procedures and Nursing Interventions
White Blood Cell Count with Differential - provide information about type of infection and the body’s response to it. -Normal is 5,000 to 10, 000 mm3. -Count less than 4, 300/mm3 is called leukopenia. It may indicate compromised inflammatory response or viral infection. - A count greater than 10, 000/mm3 indicates an inflammatory response to a pathogen or a disease process.

Differential on the laboratory report
Note: The percentage of one type of cell increases, the percent of other types decreases. Neutrophils – are among the first cells to respond to a bacterial infection. * a 70% increase in neutrophils indicates bacterial infection. This increase is often referred to as a “ shift to the left.” * A decrease in neutrophils is known as neutropenia. An overwhelming infection can deplete the bone marrow of neutrophils and produce neutropenia. Many antineoplastic drugs used to treat cancer produce bone marrow depression and can significantly lower the neutrophil count. Types of drugs that can produce neutropenia include some antibiotics, the psychotropic drug lithium, phenothiazines, and tricyclic antidepressants. Lymphocytes – are the second most commonly occuring WBC’s . Primarily respond to viral infections but also maybe elevated in case of mononucleosis, TB, and some tumors. Eosinophils – are elevated with allergic reactions and parasitic infections.

Culture and Sensitivity
Use standard precaution in collecting and handling specimens. Properly labeled and deliver promptly. Results are usually available preliminary bet hours and final results in 72 hours. If the C and S result reveals the at the cultured organism is not sensitive to prescribed antimicrobial agents, it is the nurse’s responsibility to report the result to the PCP before administering the subsequent doses of ineffective antimicrobial. An ATB that is sensitive to the organsism should be prescribed.

Erythrocyte Sedimentation Rate
ESR – The rate at which RBCs settle out of plasma. Normal adult value is between 15 to 20 mm/hr. An increase indicates an active inflammatory process or infection. Immunoglobulin Electrophoresis Determines the presence of quantity of specific immunoglobulin (IgG, IgA, IgM). Used to detect hypersensitivity disorders, autoimmune disorders, chronic viral infections, immunodeficiency, multiple myeloma, and intrauterine infections.

Antibody Screening Tests
Detect the presence of antibodies against specific causative agents. Positive antibody test indicates exposed client and developed antibodies to a specific antigen but does not indicate information whether client or not the client is currently infected (e.g. HIV antibodies). Auto-antibody Screening Test – detects the presence of antibodies against a persons own DNA (self cell). Associated with autoimmune conditions such as systemic lupus erythematosus, rheumatic arthritis.

Antigen test Detects the presence of a specific pathogen (e.g. HIV)
Used to identify certain infections or disorders. Gallium Scan A nuclear scan that uses a radioactive substance to identify hot spots of WBCs within the client’s body. Radioactive Gallium citrate is injected IV and accumulates in areas where inflammation is present. Other tests include CT scan, MRI, Biopsies to determine the presence of infection, abscesses, and lesions.

Sign and symptoms of Infections ( depends on type and organ/tissue involve.
Fever, chills Fatigue, malaise Enlarge lymph nodes Rash, skin lesions, purulent wound drainage, erythema Change level of consciousness, dysphagia, nuchal rigidity, photophobia, headache Sore throat, hyperemia, enlarge tonsils Nausea, vomiting, anorexia, abdominaal cramping diarrhea. Dyspnea, cough, purulent sputum, crackles. Dysuria, urinary frequency, hematuria, pyuria.

NANDA Nursing Diagnosis for infection
Fatigue Hyperthermia Pain (mild to moderate) Nursing Interventions Administer antipyretics for fever and discomfort as prescribed. Administer antimicrobial therapy as prescribed. Encourage increased fluid intake or maintain IV replacement to prevent dehydration. Implement infection control measures – standards, airborne, droplet, and contact. Provide diversional activities if needed. Teach the client regarding: - any infection control measures needed at home. - Self administration of medication therapy. - Complications that need to be reported immediately.

Complications Multi Drug resistant infections Sepsis
Meeting needs of Older Adult in Infections Order adults are at increased risk for infection due to: -Slowed response to ATB therapy Slowed immune response Loss of SC tissue, thinning of skin. Decreased vascularity and slowed wound healing Decreased cough and gag reflex Increased chronic illnesses Decreased gastric acid production Decreased mobility Bowel/bladder incontinence Dementia Greater incidence of invasive devices ( urinary catheter, TF, tracheostomies, IV lines.

HIV/AIDS

HIV/AIDS Human Immunodeficiency virus is a retrovirus that is transmitted through blood and body fluids. HIV Targets are CD4 lymphocytes also known as T-Cells or T-Lymphocytes. T-cells work in concert with B- Lymphocytes, both are part of specific acquired (adaptive) immunity. HIV integrates its RNA into host cell DNA through reverse transcriptase, reshaping the host’s immune system.

Human Immunodeficiency Virus Infection
Human Immunodeficiency Virus (HIV) is a retrovirus that infects cell expressing CD4 on their cell membranes primarily TH cells. The HIV copies its RNA into the host cell’s DNA and then remains quiescent until the host cell is activated to mount an immunologic response. Activation of the host TH CD4 cells also initiates replication and production of the HIV RNA which is released into the circulation. This newly made HIV then infects other TH CD4 cells

HIV Transmission - intimate sexual contact, unprotected sex (vaginal, anal, oral) - Multiple sex partners - Occupational exposure (healthcare workers) - contaminated needles ( needle sharing). - contaminated blood products (unscreen blood products) - from mother to fetus (delivery), perinatal exposure - mother to breast –feeding infant

HIV is found in different body parts and fluids:
Transmitted though blood and body fluids (semen, vaginal secretions) Found in breast milk, amniotic fluid, urine, feces, saliva, tears, CSF, lymph nodes, cervical cells, corneal tissue, and brain tissue but epidemiological studies indicated that these are unlikely sources of infection.

HIV -Stages Primary HIV-1 infection Initial Stage– 4-8 weeks – High level of virus are in the blood. Symptoms are generalized similar to flue. Marked by rapid rise in HIV viral load, decreased CD4+ cells and decreased CD8 cells CD8+ T-cells or killer T cell) belongs to a sub-group of T lymphocytes (a type of white blood cell) that are capable of inducing the death of infected somatic or tumor cells; they kill cells that are infected with viruses (or other pathogens), or are otherwise damaged or dysfunctional Resolution of clinical manifestations conincides with decline in Viral HIV copies. Lymphadenopathy persist throughout the disease process.

Latent Stage – Chronic Inactive in infected, resting, T-CD4 host cells. When the resting CD4 host is activated for an immune response, the virus begins to replicate. Levels of virus are high in the lymph nodes where TH CD4 reside but low in the blood. Maybe prolonged and clinically silent (asymptomatic) Client may be asymptomatic for 10 years or more. Anti-HIV antibodies are produced (HIV positive) Over time, the virus begins active replication using the host’s genetic machinery. - CD4 cells are destroyed, Viral load increases, and dramatic loss of immunity.

Body Response T-cells and B- cells attepmts to destroy the Th CD4 cells harvoring virus. However, the Tc cells and B cells are cripled without adequate TH CD4 support. This latent stage can last 2 to 12 years, during which time the patient is asymptomatic. During this time the number of CD4 cells declines.

Third Stage - AIDS The client begins to experience opportunistic infections. Level of TH CD4 cells are usually below 500 cells/mm3 and declining while levels of virus in the blood are increasing. Characterized by life threatening OIs. End Stage of HIV infection. This stage can last 3-5 years without treatment. Once the CD4 cells levels drops below 200 cells/mm3, the patient is considered to have acquired immunodeficiency syndrome (AIDS). Virus level in the blood is high, This stage ends in death, usually within 1 year. ALL persons with AIDS have HIV, but not all persons with HIV have AIDS.

Diagnostic Tests Antibody Essay (+ within 3 weeks to 3 months following infection) ELISA ELISA less expensive screening of HIV antibody. Positive result on an enzyme linked immunosorbent assay (ELISA) and confirmed with a positive result on a WESTERN BLOT TEST Western blot should be done to confirm the results because false positive do occur with ELISA.

CD4+ Cell Count T cell count (CD4 Test) – decreased 750 cells/mm3 Measures the extent of immune damage from HIV. Predicts disease process. Clients with values below 200 cells/mm3 have an 85% likelihood of progressing to AIDS within 3 years. The CD4 Test The main cell HIV attacks is called a T-helper cell or CD4 cell. The T-helper cell plays an important part in the immune system. It helps to coordinate all the other cells to fight illnesses. Any damage to T-helper cells can have a serious effect on the immune system.

The CD4 Test The CD4 test measures the number of CD4 or T-helper cells in the blood. The more CD4 cells in the client’s blood per cubic millimeter, the stronger the client immune system. The stronger the immune system, the better the body can fight illnesses. A low CD4 count does not mean that client will certainly become ill, but it makes it more likely.

The CD4 Test The T-helper cell has a protein CD4 on its surface.
HIV needs the CD4 in order to enter the cells it targets to infect. If HIV is able to enter the T-helper cell, it can take over the cell and then use it to duplicate itself. When HIV produces more copies of itself, the amount of CD4 cells decreases. As a result, there are fewer cells available to help the immune system to fight illnesses.

CD4 Test It is recommended that all patients with a CD4 count consistently below 200 should start antiretroviral therapy. However, data suggest that it is better to take action before the count has fallen so low. The general recommendation is for treatment to begin when the CD4 count is between 200 and 350.

Other Blood tests/Tests
CBC with Differential – abnormal – denotes anemia, thrombocytopenia, and leukopenia. Platelet count decreased – prone to bleeding. Biochemical profile – e.g. liver studies – altered for client receiving drug therapy. Brain or Lung MRI or CT scan - abnormal

Plasma HIV-1 RNA - The Viral Load Test
Viral load refers to the amount of HIV in client’s blood. The result of a viral load test indicates how much virus there is in the blood and which can harm the immune system. Increased ( > 1,5000 copies) – non detectable to highly elevated (>100, 000 copies/ml) Viral load increases coincides with active viral replication. The higher the level of HIV in client’s blood, the faster the CD4 cells are being destroyed by HIV. The lower the viral load, the stronger is your immune system. A viral load test can provide important information about the likely course of HIV infection. There are different viral load tests available. Each of them uses a different technique to measure the amount of HIV in the blood. The results from the different tests tell you whether the viral load is low medium or high.

Major complications Opportunistic Infections
fungal (candida albicans /thrust); red bleeding gums and oral mucuous membranes. Bacterial Infections – Mycobacterium avium/tuberculosis. Protozoan Infections - PCP, cryptosporidium, toxoplasmosis Viral Infections – cytomegalovirus (lung inflammation, colitis, blindness); Herpes Simplex virus – painful vascular lesions, seizures, blindness, deafness. Wasting Syndrome – secondary to OP, malnutrition. Secondary cancers (Kaposi sarcoma – purplish or brown lesions Non-Hodkin’s B –Cell lymphomas (weight loss, fever, night sweats) Dementia

Pt. With AIDS are high risk for Opportunistic Infections
Fungal ( thrust)- Oral candidiasis Parasitic - Viral Infection – Herpes Simplex Cytomegalovirus retinitis Pneumocystis carinii Pneumonia Cryptosporidium enteritis Cryptococcus neoformans meningitis Toxoplasmosis.

Pt. With AIDS are high risk for cancers (40%) of patient with HIV
Kaposi’s sarcoma Non-Hodgkin’s Lymphoma Anal cancer Cervical cancer CNS effect Encephalophaty Cognitive impairment Dementia

Sign and Symptoms Initial stage – general flu-like symptoms
Second and latent stage – may not experience any symptoms Third stage – Pt may present for medical care complaining of frequent persistent symptoms Fever, night sweats, swollen lymph nodes, or other symptoms specific to the site of infection such as headache, skin lesions that do not heal, sore throat, dyspnea, Burning with urination, or diarrhea. Extreme fatigue and weight Loss Any of these symptoms coupled with Hx unprotected Sex with person possibly infected with HIV, Hx of IV drug abuse using shared needles, or a history of a blood transfusion before 1989 warrants consideration of diagnosis of HIV

Medical Treatment There is no cure for HIV. The medical treatment of HIV infection is symptomatic and aimed at reducing the viral load, preventing and treating infections and treating malignancies. Early stages – outpatient treatment Maintain balance diet Exercise regularly Maintain good dental hygiene Stop smoking and using illicit drugs Minimize stress And practice safe sexual habits.

NANDA NURSING DIAGNOSIS
Risk for infection Imbalanced Nutrition: less than body requirements Fatigue/activity Intolerabce Fluid Volume Deficit Ineffective Coping Ineffective therapeutic regimen management.

Nursing Interventions
Provide Client teaching - Transmissions, infection control measures, safe sex practices. Need for well balanced diet, self administration of prescribed medications and potential s/e. s/s that need to be reported immediately (infection). The need for frequent follow-up monitoring CD4 and viral count. Identify factors that may interfere with nutrition and correct if possible Encourage activity alternated with rest periods Administer supplemental Oxygen as needed Provide analgesia as needed. Provide skin care as needed/ Emphasize the importance of carefully complying with anti-retroviral dosing schedules. Encourage use of constructive coping mechanisms. Assist the client with identifying primary support systems. Refer the client to local AIDS support groups as appropriate.

Opportunistic Infections Management
Implement and maintain anti-retroviral drug therapy as prescribed. (HARRT- highly active antiretroviral therapy) Protease Inhibitor – Indinavir, Saquinavir Nucleoside reverse transcriptase inhibitors – didasone, zidovudine. Nonnucleoside reverse transcriptase inhivitors – nevirapine, delavirdine Antineoplastic-interferon alpha 2a, interferon alpha 2 b Antibiotics – Isoniazid, azithromycin, ripamfin Antifungals – amphotecirin B, Fluconazole Antidiarrheals – diphenoxylate HCL, atropine Antidepressant – Paroxetine, sertraline Analgesics – Opioids, NSAIDS Appetitte stimulants ( Megace) Antivirals – ganciclovir.

Monitor for skin breakdown Maintain fluid intake Maintain nutrition Teach client to report s/s of infection immediately to PCP. Wasting syndrome – Maintain nutrition orally or by TPN if indicated. Provide between meal supplemental snack. Serve at least six small frequent feedings with high value protein. Fluid/Electrolyte Imbalance – Monitor fluid/electrolyte status. Report abnormal lab. Data promptly, Maintain IV fluid replacement. Seizures (HIV encephalopathy) maintain client safety. Implement seizure precautions.

HIV Structure These pictures show the structure of the Human Immunodeficiency Virus (HIV). The outer shell of the virus is known as the viral envelope. Embedded in the viral envelope is a complex protein known as env, which consists of an outer protruding cap glycoprotein (gp) 120, and a stem gp41. Within the viral envelope is an HIV protein called p17 (matrix), and within this is the viral core or capsid, which is made of another viral protein p24 (core antigen). The major elements contained within the viral core are two single strands of HIV RNA, a protein p7 (nucleocapsid), and three enzyme proteins, p51 (reverse transcriptase), p11 (protease) and p32 (integrase).

Nucleoside Analogs - NRTIs
AIDS drugs known as nucleoside analogues. The first group of antiretroviral drugs are the Nucleoside Reverse Transcriptase Inhibitors (NRTIs). They were the first type of drug available to treat HIV and AIDS in 1987 and are better known as nucleoside analogues or nukes. HIV needs an enzyme called reverse transcriptase in order to be able to infect healthy cells and reproduce itself in a person's body. As the name says, NRTIs inhibit reverse transcriptase. The drugs slow down the production of the reverse transcriptase enzyme and make HIV unable to infect cells and duplicate itself.

Protease Inhibitors - PIs
Protease inhibitors (PI). They were first approved in 1995. Protease inhibitors, as the name says, inhibit protease. Almost every living cell contains protease. Protease is a digestive enzyme that breaks down protein and is one of the many enzymes that HIV uses to reproduce itself. The protease in HIV attacks the long healthy chains of enzymes and proteins in the cells and cuts them into smaller pieces. These infected smaller pieces of proteins and enzymes continue to infect new cells. The protease inhibitors take effect before the protease in HIV has the chance to break down the protein and enzymes. This way the protease inhibitors slow down the duplication of the virus and thus prevent the infection of new cells. The NRTIs and NNRTIs only have an effect on newly infected cells. Protease inhibitors are able to slow the process of immature non-infectious virus becoming mature and infectious. Protease inhibitors also work in cells that have been infected for a long time, by slowing down the reproduction of the virus.

Antiretroviral treatment
Antiretroviral treatment for HIV infection consists of drugs, which work against HIV infection itself by slowing down the reproduction of HIV in the body. The drugs are often referred as antiretrovirals, anti-HIV drugs or HIV antiviral drugs

AZT - Antiviral Medication
This is a picture of AZT, the first approved antiretroviral drug for treatment of HIV and AIDS. In March 1987, the U.S Food and Drug Administration (FDA) approved AZT to be used as a treatment for AIDS.

CANCERS

Cancer – Neoplastic Disease Process
Abnormal cell growth and differentiation Exact cause – unknown Cancer cells invade surrounding tissues and spread to other areas. Trigger factors may include viruses, physical and chemical agents, hormones, genetic and diet. Carcinomas – epithelial tissues Adenocarcinomas – glandular glands Sarcomas – mesenchymal tissues Leukemias – malignancies of blood forming cells Lymphomas – lymph tissues Multiple myeloma – plasma cells and affects the bone.

Risk Factors Age Genetic Predispositions
Exposures t chemicals, viruses, tobacco, and alcohol Diet high in fat and red meat, low in fiber Sun, ultraviolet light, or radiation exposure, (radon) Sexual lifestyle, Multiple sexual partners, STD, HIV/AIDS Other risk factors are poverty, obesity, and chronic GERD

Diagnostic Procedure Tissue biopsy – definitive diagnosis of abnormal cancer cells. CBC and Differential – screening for leukemias Chest X-Ray, CT scan, MRI, PET scan – visualized tumors, metastasis or progression of cancer. Tumor Marker Essay – CEA,CA 124, Alphafetoprotein) – screening for cancers of the colon, pancrease, prostate, liver, uterus, and ovaries. Elevated values suggestive of cancer.

Therapeutic procedures
Radiation – ionizing radiation of tissue by the path of the radiation beam resulting to death of cells. S/E include skin changes, hair loss, and debilitating fatigue. Internal Radiation Therapy- - Client should be place on a private room and bath - Appropriate signage should be place on the door warning of the radiation source. - healthcare personnel should wear a dosimeter film badge that records the amount of radiation exposure. - visitors should be limited to 30 min visits and maintain distance of 6 feet. - Visitors and health care personnel who are pregnant or under the age of 16 should not come in contact with the client. - A lead container should be kept in the client’s room if the delivery method could allow spontaneous loss of radioactive material. - Precautions listed above should be carried out at home if the client is discharge during therapy.

External Radiation Wash skin over irradiated area gently with mild soap and water and dry thoroughly using patting motions. Do not remove radiation “tattoos” that are used to guide therapy. Do not apply powders, ointments, lotions or perfumes to irradiated skin. Wear soft clothing over irradiated skin and avoid tight or constricting clothes. Do not expose irradiated skin to sun or heat source.

Surgical Excision Diagnostic , curative, or palloative. Risk of seeding. Chemotherapy certified provider administers systemic or local cytotoxic medications to destroy rapid dividing cells. Often combination of anticancer medications are used and significant adverse effect is IMMUNOSUPPRESSION ( bone marrow supression). measures must be employed to reduce the risk especially at the medications “nadir”. Nausea and vomiting, alopecia, and mucositis are common side effects. Take measures to prevent extravasation of vesicants.

Sign and Sypmtoms CAUTION C – change in bowel or bladder habits
A – a sore that does not heal U – unusual bleeding or discharge T- thickening of a lump in the breast or elsewhere I – Indigestion or difficulty swallowing O- obvious change in warts or moles N- nagging cough or hoaseness Weight loss Fatigue and weakness Pain Nausea and anorexia.

NANDA Nursing Diagnosis
Anticipatory grieving Risk for infection Fear/anxiety Imbalanced Nutrition: Less than body requirements Ineffective Tissue perfusion

Encourage screenings (pap smears , mammogram, colonospcopy, stool for OB) Implement pain control measures as prescribed. Encourage /maintain fluid intake – premdedicate prior to eating antinausea (odansetron- Zofran) administer appetite stimulant (megace)m add protein powder to feedings. Reduced risk for Neutropenia Protect client from possible source of infection. Use hand hygiene Avoid crowds while undergoing chemotherapy Administer colony-stimulating factors Neupogen – stimulate WBC production.

Reduce risk of anemia administer recombitant erythropoeitin alpha as prescribed. Reduce risk of Thrombocytopenia – avoid NSAIDs and IM injections if platelet count is decrease. Maintain IV fluids Implement post-radiation care if applicable Interventions are based on site of radiation. Antidiarrheals for GI Tract, Mouthcare for head and neck, administer Octrotide ( Sandostine) as prescribed. Encourage female client to wear hat or wig if undergoing radiation or chemotherapy that produces alopecia. Children – offer a baseball LISTEN TO CLIENT’s CONCERN Avoid false reassurance Allow time to disscuss feelings regarding loss and grieve.

Complications and Nursing Implications
Oncologic Emergencies Syndrome of Inappropriate Antidiuretic Hormone ( SIADH). Monitor hyponatremia and serum osmolality. Administer Lasix IV, IV NS and/or Hypertonic saline as prescribed for severe hyponatremia. Spinal Cord Compression – related to metastasis. Assess the client’s neurological status, including motor, and sensory deficits. Administer corticosteroid as prescribed. Support the client during radiation therapy. Hypercalcemia Superior vena cava Syndrome – Position in high Fowler’s position. Dissiminated intravascular Coagulation – Observe the client for bleeding and apply pressure as needed.

Autoimmune Disorders Normally, the immune system recognizes that the tissues in the body are not "foreign" and does not attack them. If a transplant is performed, however, the immune system usually recognizes that the organs that are transplanted are different and attacks them, a process called rejection. Drugs that reduce the activity of the immune system (immunosuppressants) are typically given to persons who have received transplants, unless the donor is an identical twin. Cancer cells are sometimes different enough from normal cells that the immune system attacks them, but the immune response alone is usually not enough to keep a cancer from spreading.

What are autoimmune disorders?
Autoimmune disorders are diseases caused by the body producing an immune response against its own tissues. The cause of autoimmune diseases is unknown, but it appears that there is an inherited predisposition to develop autoimmune disease in many cases. In a few types of autoimmune disease (such as rheumatic fever), a bacteria or virus triggers an immune response, and the antibodies or T-cells attack normal cells because they have some part of their structure that resembles a part of the structure of the infecting germ.

Localized Autoimmune Diseases
Rheumatoid arthritis (joints; less commonly lung, Lupus [Systemic Lupus Erythematosus] (skin, joints, kidneys, heart, brain, red blood cells, other) Scleroderma (skin, intestine, less commonly lung) Sjogren's syndrome (salivary glands, tear glands, joints) Wegener's granulomatosis (sinuses, lungs, kidneys) Primary biliary sclerosis, Sclerosing cholangitis, Autoimmune hepatitis (liver) Polymyalgia Rheumatica (large muscle groups) Temporal Arteritis / Giant Cell Arteritis (arteries of the head and neck) skin)

Systemic Autoimmune Diseases
Type 1 Diabetes Mellitus (pancreas islets) Hashimoto's thyroiditis, Graves' disease (thyroid) Celiac disease, Crohn's disease, Ulcerative colitis (GI tract) Multiple sclerosis, Guillain-Barre syndrome (central nervous system) Goodpasture's syndrome (lungs, kidneys) Addison's disease (adrenal) Raynaud’s phenomenon (fingers, toes, nose, ears)

Rheumatoid Arthritis Is a chronic, systemic, progressive inflammatory disease of the synovial tissue. A bilateral systemic inflammatory disease process involving multiple joints. Classified as an autoimmune disease process which antibodies are formed against synovial tissues include synovial membrane, articular cartilage, joint capsule, tendon and ligaments surrounding the joints, involvement of the disease is one of exacerbations and remissions. The natural course of the disease is one of exacerbations and remisions. Inflammation and tissue damage can cause severe deformities that greatly restrict function.

Risk Factors Female gender Age 20 to 50 years Genetic Predisposition
Epstein Barr Virus - The Epstein-Barr Virus (EBV), also called Human herpesvirus 4 (HHV-4), is a virus of the herpes family (which includes Herpes simplex virus and Cytomegalovirus ), and is one of the most common viruses in humans. Most people become infected with EBV, which is often asymptomatic but commonly causes infectious mononucleosis.

Diagnostic Procedures
Diagnostic Procedures and Nursing Interventions Rheumatoid Factor ( RF) antibody Diagnostic for Rheumatoid Arthritis + 1:40 to 1:60 ( normal < 1:20 Antinuclears Antibody ( ANA) titer ( antibody produced against one’s own DNA) high titer correlate with severe disease. A ( +) ANA titer is associated with RA ( normal is negative ANA titer at 1:20 dilution). Erythrocyte Sedimentation Rate (ESR) : ELEVATED 20 – 40 mm/hr = mild inflammation 40 – 70 mm/hr = moderate inflammation mm/hr = severe inflammation

Arthrocentesis Synovial fluid aspiration by needle
With RA, increased white blood cells ( WBC) and RF are present. S/S (clinical findings depend on the area affected by the disease process) - Pain at rest and with movement - Morning stiffness - joint deformity - Anorexia/weight loss - Fever ( generally low grade) - Fatigue - Muscle weakness/atrophy What to assess or monitor? Pain ( character, intensity, effectiveness of relief measure) Functional ability Indications of infections

NANDA NURSING Diagnosis
Fatigue Impaired physical mobility Chronic pain Disturbed body image Risk for injury

Apply heat or cold to areas affected as indicated based on client response. Morning stiffness (hot shower) Pain ( heated paraffin) Edema ( cold therapy) Assist with and encourage physical activity to maintain joint mobility ( w/in capabilities of the client) Maximize functional activity, minimize pain, conserve energy ( pacing activities and rest periods) Provide a safe environment - facilitte use of assistive device. Utilize progressive muscle relaxation. Monitor the client for s/s of fatigue. Refer the client to support groups as appropriate

Administer medications as prescribed. Analgesics Anti-inflammatories – NSAIDS e.g. Plaquinel (hydroxychloroquine), Azulfidine (sulfasalazine) Steroid e.g. Prednisolone ( Prednisone) – monitor for fluid retention , HTN and renal dysfunction. Immunosuppressants - slow the progression of disease e.g. Methotrexate ( rheumatrex), cyclophosphamide( Cytoxan), Leflunomide ( e.g Arava). Monitor for toxic effects ( bone marrow suppressions, increased liver enzymes).

Administer Biological response Modifiers – inhibit the action of tumor necrosis factor ( TNF) - E.g etanercept ( Enbrel), infliximab ( Remicade), adalimumab (Humira) and Anakinra ( kineret) - Do not administer if client have serious infection. - Monitor for injection/infusion reactions - Monitor CBC and the client for signs of infections. Monitor for medication effectiveness ( reduced pain, increased mobility) Teach the client regarding s/s that needs to be reported immediately ( fever, infection).

Complications and Nursing Implications
Sjoren’s syndrome ( dry eyes, dry mouth, dry vagina) Joint deformity ( tendon rupture, secondary osteoporosis). Vasculitis ( ischemic organs) Cervical sublaxation ( risk of quadriplegia and respiratory compromise).

GENETICS

Genetics Genetics has profound impact on health and disease.
More than 4000 diseases are though to be related to mutated genes. Common disorders like heart diseases and most cancers arise from a complex interplay among multiple genes and between genes and factors in the environment. The study of principles of genetics is very important to nursing. The ability to know basic genetic principles will enable nurses to become prepared to assist the patient and their family in dealing with genetic issues.

Basic Principles of Genetics
Genes are transmitted from parents to their offspring. Genes are basic units of heredity – approximately 20,000 to 25,000 genes in each person’s genetic make-up or genome. Any change in gene structure leads to a mutation that may alter the type and amount of protein produces. Each gene has a specific location on a chromosome termed a locus. Alelle is one of two or more alternative forms of a gene that occupy corresponding loci on homologous chromosomes.

Basic Principles of Genetics
Chromosomes are contained in the nucleus of the cell and occurs in pairs. There are 23 pairs of chromosomes and are said to be homologous and are termed autosomes. Autosomes are the same is males and females. The sex-chromosomes make-up the 23rd pair of chromosomes. A female has two X chromosomes. A male has one X and one Y chromosomes. One chromosome of each pair is inherited from the mother and the father. The sperm cell of the father carries either a X or Y chromosomes.

Basic Principles of Genetics - DNA
DNA – Genes are made up of a nucleic acid called deoxyribonucleic acid that stores genetic information and encodes the instruction for synthesizing specific proteins needed to maintain life. DNA also dictates the rate at which protein will be made. DNA is made up of 4 nitrogeneous bases known as adenine, thymine, guanine, and cytosine.

Basic Principles of Genetics- RNA
Ribonucleic acid is very similar to DNA . Lack thymine and instead contains uracil. RNA is single stranded and contains ribose instead of deoxyribose sugar. RNA transfers the genetic information obtained from DNA to the proper location for protein synthesis and plays a critical role during synthesis of protein. Protein synthesis – transcription and translation. Human Genome Project – initiated in 1990 and completed in 2003 is international effort to map all 20,000 to 25,000 human genes and determine the complete sequence of more than 3 billion DNA bases.

Basic Principles of Genetics - Alleles
When two gene pairs are different alleles, the allele that is fully expressed is the dominant allele. The other allele that lacks the ability to express itself in the presence of a dominant allele is the recessive allele. Physical traits expressed by a person are termed the phenotype, and the actual genetic makeup of a person is termed as genotype. Cell Division Mitosis – results in formation of genetically identical daughter cells. Meiosis – occurs in sexual reproductive cells. Nondisjunction – results to disorders such Down Syndrome and Turner Syndrome. These disorders are characterized by physical and/or mental defects.

Disorders Resulting from Nondisjunction
Nondisjunction – failure of the two chromosomes to separate during meiosis causing an abnormal number of chromosomes. The oocyte or the sperm may have two copies of the same chromosomes or missing one. Down Syndrome - trisomy 21, or trisomy G, is a chromosomal disorder caused by the presence of all or part of an extra 21st chromosome. Often Down syndrome is associated with some impairment of cognitive ability and physical growth , and a particular set of facial characteristics. Down syndrome in a fetus can be identified with amniocentesis during pregnancy, or in a baby at birth. Individuals with Down syndrome tend to have a lower than average cognitive ability, often ranging from mild to moderate developmental disabilities.

Turner Syndrome Turner syndrome or Ullrich-Turner syndrome (also known as "Gonadal dysgenesis" encompasses several conditions, of which monosomy X (absence of an entire sex chromosome) is most common. It is a chromosomal abnormality in which all or part of one of the sex chromosomes is absent (unaffected humans have 46 chromosomes, of which two are sex chromosomes). Typical females have two X chromosomes, but in Turner syndrome, one of those sex chromosomes is missing or has other abnormalities. In some cases, the chromosome is missing in some cells but not others, a condition referred to as mosaicism or 'Turner mosaicism'.

Inheritance Pattern Genetics disorders can be categorized into autosomal dominant, autosomal recessive, or sex-linked (x-linked) recessisve disorders If the mutant gene is located on an autosome, the genetic disorder is called autosomal. If the mutant gene is located on the x-chromosome, the genetic disorder is called x-linked.

Autosomal Dominant Disorders
Caused by mutation of a single gene pair (heterozygous) on a chromosome. Dominant allele prevails over a normal allele. Shows variable expression. Variable expression means that the symptoms expressed by the individual with the mutual gene vary from person to person even if they have the same mutated gene. Although autosomal dominant disorders have a high probability of occurring in families, sometimes these disorders caused a new mutation or skip a generation. This is called incomplete penetrance.

(The Pediatric Orthopaedic Society of North America 2010 ( Autosomal dominant disorders are relatively commonly seen in orthopedic practice. Affected individuals are heterozygous, with one normal and one mutated gene. Since the mutated gene determines phenotypic expression, the disorder is characterized as dominant. Homozygosity is generally fatal. Variable expressivity is characteristic of autosomal dominant disorders. Transmission is characterized by one half of offspring of affected individuals being affected, regardless of sex. Examples of autosomal dominant disorders are achondroplasia, pseudoachondroplasia, the multiple epiphyseal dysplasias, chondrodysplasias, osteogenesis imperfecta, Marfan syndrome, polydactyly, hereditary motor sensory neuropathies I and II (Charcot-Marie-Tooth disease), myotonic dystrophy, and neurofibromatosis. A common feature of autosomal dominant disorders is that they are structural disorders. While they may impair function and have some reduction in life expectancy, survival to at least reproductive age is the rule.

In the case of autosomal dominant genes, a single abnormal gene on one of the autosomal chromosomes (one of the first 22 "non-sex" chromosomes) from either parent can cause the disease. One of the parents will have the disease (since it is dominant) in this mode of inheritance and that person is called the CARRIER. Only one parent must be a carrier in order for the child to inherit the disease.

Common Diseases on each category
Autosomal Dominant: - Huntington’s Disease - Familial Hypercholesterolemia - Neurofibromatosis - Breast and Ovarian Cancer elated to BRCA genes - Marfan Syndrome - hereditary nonpolyposis colorectal cancer Autosomal Recessive: - Cystic Fibrosis - Tay-Sach’s Disease - Phenylketonuria - Sickle –Cell Disease - Thallasemia Sex-linked Recessive - Hemophilia - Duchenne Muscular Dystrophy - Wiscott-Aldrich Syndrome

Gene Therapy

Autosomal Recessive Disorders
Are caused by mutation of two gene pairs (homozygous) on a chromosomes. A persons who inherits one copy of the recessive allele does not develop the disease because the normal allele predominates. However such person is a carrier. The risk of two heterozygotes, or carriers, having an affected child is 25%, 1 in 4, for each child that they have. On the contrary, there is a 3 in 4 chance that each child will not be affected. Males and females are at equal risk for being affected. Two affected individuals usually produce children all of whom are affected as well.

Autosomal Recessive Disorders

X-linked Recessive Disorders
They are caused by mutation of the X-chromosomes. Usually men are affected by this disorder because women who carry the mutated gene on one X-chromosome have another X chromosome to compensate for the mutation. However, women who carry the mutated gene can transmit the mutated gene to their offspring.

X-linked Diseases X-linked diseases usually occur in males. Males have only one X chromosome. A single recessive gene on that X chromosome will cause the disease. The Y chromosome is the other half of the XY gene pair in the male. However, the Y chromosome doesn't contain most of the genes of the X chromosome. It therefore doesn't protect the male. This is seen in diseases such as hemophilia and Duchenne muscular dystrophy . TYPICAL SCENARIOS For a given birth, if the mother is a carrier (only one abnormal X chromosome) and the father is normal: 25% chance of a normal boy 25% chance of a boy with disease 25% chance of a normal girl 25% chance of a carrier girl without disease If the father has the disease and the mother is normal: 100% chance of a normal boy 100% chance of a carrier girl without disease

X-linked Diseases X-LINKED RECESSIVE DISORDERS IN FEMALES
Females can get an X-linked recessive disorder, but this is very rare. An abnormal gene on the X chromosome from each parent would be required, since a female has two X chromosomes. This could occur in the two scenarios below. For a given birth, if the mother is a carrier and the father has the disease: 25% chance of a healthy boy 25% chance of a boy with the disease 25% chance of a carrier girl 25% chance of a girl with the disease If the mother has the disease and the father has the disease: 100% chance of the child having the disease, whether boy or girl. The odds of either of these two scenarios are so low that X-linked recessive diseases are sometimes referred to as “male only” diseases. However, this is not technically correct. Female carriers can have a normal X chromosome that is abnormally inactivated. This is called "skewed X-inactivation." These females may have symptoms similar to those of males.

Multifactorial Inhireted Conditions
These are caused by a combination of genetic and environmental factors. These disorders run in the families but do not show the same inherited characteristics as the single-gene mutation conditions. Mutifactorial conditions are poorly understood but include Diabetes Millitus, Obesity, Hypertension, Cancer, and Coronary Artery Diseases

Gene Therapy Is an experimental technique that is used to replace or repair defective or missing genes with normal genes. It is currently only being tested for the treatment of diseases that have no other cures Started with gene therapy trials in children with severe combined immunodeficiency disease caused by adenosine deaminase deficiency. T Lymphocytes from these children were obtained, and the missing gene was inserted into these T Cellsto produce the missing enzymes, and these children were capable of developing a functioning immune system.

Nursing Management The role of the nurse in Genetics is to be able to assist client and family in making critical decision related to genetic issues such as genetic testing. Collaborate with the team or physician to involve a genetic counselor. Give client and families accurate information pertaining to genetics, genetic diseases and probabilities of genetic disorders. (See Punnet squares figure 14.4 Lewis pp. 218.

Stem Cells Use of stem cells may allow for regeneration of lost tissue and restoration of function in diseases such as Parkinson’s Disease, Alzheimer’s Disease, Heart Disease, Diabetes Millitus and Spinal Cord Injuries. Stem cells in the body that have ability to differentiate into other cells. Stem cells can be divided into two types: embryonic and adult. Embryonic stem cells have the ability become anyone of the hundred of types of cells in the human body. Adult stem cells – are undifferentiated cells that are found in small numbers in most adult tissues. Found in children and can be extracted from umbilical cords. Their role in the body are to maintain and repair tissues in which they are found. Multipotent cells.

Normal Immune Response
Immunity is a state of responsiveness to foreign substances such as microorganisms and tumor proteins. Immune Response serves three functions: Defense – The body protects against invasion by microorganisms and prevents the development of infection by attacking 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.

Types of Immunity Innate ( Natural) Acquired
Innate immunity exist in a person without prior contact with an antigen. Involves nonspecific response and neutrophils and monocytes are primary WBC involved. Ex. Species specificity of infectious agents Acquired Immunity – is the development of immunity, either actively or passively.

Types of Immunity Active Acquired Immunity – results from the invasion of the body by foreign substances such as microorganisms and subsequent development of antibodies and sensitized lymphocytes. With each reinvasion of the microorganisms, the body responds more rapidly and vigorously to fight off the invader. May results naturally from a disease or artificially through inoculation of a less virulent antigen (e.g. immunizations). Immunity develop on this is long lasting.

Active Acquired Immunity
e.g. Natural contact with antigen through clinical infection (from chickenpox (varicella), measles (rubeola), and mumps). e.g. Artificial – immunization with antigen (immunization with live attenuated virus or killed vaccines). E.g. MMR, DTaP, HAV, HBV.

Passive Acquired Immunity
Implies that the host receives antigen rather than synthesizing them. This may take place naturally through the transfer of immunoglobulins across the placental membrane from the mother to fetus. Artificial passive acquired immunity occurs through injection with gamma globulin ( serum antibodies). Immunity provides immediate benefits but passive immunity is short lives because the host did not synthesize the antibodies and consequently does not retain memory cells for the antigen.

Antigens Substance that elicit an immune response.
Most are composed of protein. Some are large polysaccharides, lipoproteins, and nucleic acids. All of the body organs have antigens on their surface that are unique to each person and enable the body to recognize itself. The immune system becomes “ tolerant” to the body’s own molecules and therefore nonresponsive to “self” antigens.

Lymphoid Organs The lymphoid system is composed of central and peripheral lymphoid organs. Central lymphoid organs are the thymus glands and bone marrow. Peripheral lymphoid organs are the tonsils, gut, genital, bronchial, and skin associated lymphoid tissues, lymph nodes, and spleen.

Lymphocytes They are produced in the bone marrow and eventually migrate to the peripheral organs. Thymus is important in the differentiation and maturation of T-Lymphocytes therefore essential for a cell- mediated immune response. Thymus is large during childhood and shrink with age. Tonsils are typical lymphoid tissue. Skin associated lymphoid tissue – Lymphocytes and Langerhans cells. When Langerhans cells are depleted, the skin can neither initiate an immune response nor support a skin localized delayed hypersensitivity response.

Lymphocytes Antigens introduced to the body.
Antigens interact with B and T Lymphocytes and macrophages in the lymph nodes. Lymph nodes – filter foreign material brought to the site and circulation of lymphocytes. Spleen – is important as the primary site for filtering foreign substances from the blood. Consist of white pulp containing B and T lymphocytes and red pulp containing RBC. Macrophages line the pulp and sinuses of the spleen. The spleen therefore is the major site of immune response for blood-borne antigens.

Cells Involved in Immune Response
Mononuclear Phagocyte – Monocytes in the blood and macrophages. Mononuclear phagocytes have critical role. Involve in capturing, processing, and presenting the antigen to the lymphocytes. Stimulates humoral or cell-mediated immune response. Macrophage –bound antigen (highly immunogenic) is presented to circulating T or B Lymphocytes and thus triggers an immune response.

Lymphocytes B Lymphocytes – produced from bone marrow. Differentiate into plasma cells when activated. Plasma cells produced antibodies (immunoglubolins). T Lymphocytes – cells that migrate from bone marrow to thymus to differentiate into T – Lymphocytes. Thymosin – helps in maturation and differentiation of T-Lymphocytes. T-Lymphocytes are primarily responsible for immunity to intracellular viruses, tumor cells, and fungi. T-Lymphocytes are categorized into T cytotoxic and T helper cells.

T-Cytotoxic Cells Also known as CD8 cells are involve in attacking antigens on the cells membrane of foreign pathogens and releasing cytolytic substances that destroy the pathogen. Have antigen specificity and are sensitized by exposure to antigen. They can also remain as a memory T-Cell. Sensitized T-cells that are not attacking. Provides more rapid and intense cell-mediated immune response on the 2nd exposure.

T-Helper Cell Also known as CD4 cells involved in the regulation of cell-mediated immunity and the humoral antibody response. Differentiates into subsets and produce distinct cytokines TH2 and TH1 cells. TH1 cells – stimulates phagocyte mediated immunity. TH2 cells – stimulates phagocytes independent, eosinophil-mediated immunity which is effective against parasites. Also involve in allergic response.

Natural Killer Cells NK Cells are also involved in cell-mediated immunity. These cell are not T or B cells but are large lymphocytes with numerous granules in the cytoplasm. NK Cells do not require prior sensitization for their generation. Involve in killing of virus infected cells, tumor cells, and transplanted grafts. Has significant role in immune surveillance for malignant changes. Dendritic Cells- important in cell mediated immune response. Called Langerhans cells in the skin. Found in lining of the nose, lungs, stomach, and intestine. Dendrites capture antigens at site and then transport the antigen until it encounters a T Cell with specificity for the antigen.

Cytokines Soluble factors secreted by WBC and other cells in the body that acts as messengers between the cell types. See page 222 of Lewis for Types and Functions of specific Cytokins . Types Interleukin (Ils) - Interferons Tumor Necrosis Factor (TNF) Colony stimulating Factors ( CSFs) Erythropoietin

Cytokines Have a beneficial role in hematopoiesis and immune function. They can also have detrimental effects such as those seen in chronic inflammation, autoimmune diseases and sepsis. There are currently at least 100 different cytokines. They acts as immunomodulatory factors, colony-stimulating factors acts as growth regulating fasctors for hematopoeietic cells, and interferons are antiviral and immunomodulartory.

Comparison of Humoral and Cell-Mediated Immunity
Humoral Immunity - consist of antibody-mediated immunity. Production of antibody is an essential component in a humoral immune response. Cell –Mediated Immunity – Immune response are initiated through specific antigen recognition by T cells. The cell types involve include T lymphocytes, macrophages, and NK cells. Cell – mediated immunity is of primary importance in 1. immunity against pathogens that survive inside of cells, including viruses and some bacteria 2. fungal infections 3. rejection of transplanted tissues 4. contact hypersensitivity reactions 5. tumor immunity

Altered Immune Response
Hypersensitivity reactions – occurs when the body fails to recognize self-protein. ( see Lewis pg. 225 table 14-9. Type 1 – IgE – mediated reactions – pollens, food, drugs , dust. Involve antibody - IgE Type II – Cytotoxic Reactions – cells surface of RBC’s basement membrane IgG, IgM frequently. Type III – Immune Complex Reactions – Extracellular fungal, viral, bacterial. IgG, IgM Type IV _ Delayed Hypersensitivity Reactions – intracellular or extracellular. NO antibody involve.

Emergency Management for Anaphylactic Shock
Etiology – injection of, ingestion of, or topical exposure to substance that produces profound allergic response. Initial - Ensure patent airway - remove insect stinger if present. - Epinephrine 1:1000, 0.2 – 0.5 ml SC for mild symptoms; repeat at minutes intervals. - Epinephrine 1:10,000, 0.5 ml IV at 5 to 10 minte intervals for severe reactions. - administer high flow oxygen via non-rebreather mask. - Place recumbent and elevate legs. - Keep warm. - administer Diphenhydramine ( Benadryl) IM or IV Administer histamine H2 blocker such as Cimetidine ( Tagamet) Maintain blood pressure with fluids, volume expanders, vasopressors, e.g. dopamine ( Intropin), norepinephrine bitartrate (Levophed). Ongoing Monitoring Monitor V/S , respiratory effort, O2 sat, LOC, and Cardiac rhythm. Anticipate intubation with severe Respiratory distress. Anticipate cricothyrotomy or tracheostomy with severe laryngeal edema.

Graft versus Host Disease
Graft vs. Host Disease occurs when an immunoincompetent (immunodeficient) pt. is tranfused or transplanted with immunocompetent cells. In transplantation the biggest concern is host’s rejection of the graft. The GVH response may have its onset 7 to 30 days after transplantation. It involves donor T-cells attacking and destroying vulnerable host cells. No adequate treatment of GVH disease once it is established. Corticosteroid are often used. They enhance susceptibility to infection. The use of immunosuppressive agents has been most effective as a preventive rather than a treatment measure. Radiation of blood products before they are administered is another measure to prevent T cell replication.

Organ Transplantation
Organs that can be transplanted: - Cornea - Heart valves - Lungs - Kidneys - Small intestine - Pancreas/Islets cell - Tendons/Cartilages - Bone/Bone marrow - Skin

Donor Sources Cadaver Living Donors
How to be come a donor. The individual has to notify the state of his/her decision when receiving a new driver’s license. Will receive an organ donor card. An organ donor should also notify his/her family because the family members are ultimately the people who give the medical community the approval to enroll a deseased individual as an organ donor.

Requirement: Donor and Recipient Matching
Factors to consider for matching: ABO Blood and human leukocyte antigen ( HLA) typing, medial urgency, time on the waiting list, and geographic locations Histocompatibility studies – to identify the HLA for both donors and potential recipients.(PCR test is done to type for the antigens at all five loci (A,B,C,D, and DR)

Transplant Rejection Hyperacute rejection – occurs minutes to hours after transplantation. No treatment. Organ is removed. Acute rejection – most commonly occurs days to month after transplantation. This type of rejection is mediated by the recipients T-cytotoxic lymphocytes which attack the foreign organ. Immunosuppressive Therapy helps. Long term used of immunosuppressants place clients in high risk for infections for a longer period of time. Chronic rejection – is a process that occurs over months or years and is irreversible. No definitive therapy for this type of rejection. Treatment is mainly supportive. 7Please read pg. 239 Lewis for Drug Therapy used for Immunosuppressive Therapy.

NUR 120 Week 6 Immune Disorders Infection Human Immunodeficiency Virus

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NUR 120 Week 6 Immune Disorders Infection Human Immunodeficiency Virus

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