Nursing 498 Winter 2025 Immunity PDF

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Uploaded by BestSellingBowenite7551

University of Calgary

2025

Nursing

Catherine Fox, Robyn Dhanoa, Shelley de Boer

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immunology immune disorders drug therapy nursing

Summary

This nursing presentation covers various aspects of immune disorders and the associated drug therapies. It details the mechanisms of action, potential adverse effects, and drug interactions for different types of immunosuppressants, including corticosteroids and others. The document also highlights the importance of nursing assessment and patient education.

Full Transcript

IMMUNITY Nursing 498 Winter 2025 Catherine Fox Robyn Dhanoa Shelley de Boer Objectives Identify safe, effective, nursing management of Select and prioritize pharmacological nursing outcomes and interventions for...

IMMUNITY Nursing 498 Winter 2025 Catherine Fox Robyn Dhanoa Shelley de Boer Objectives Identify safe, effective, nursing management of Select and prioritize pharmacological nursing outcomes and interventions for interventions to develop individuals across the a plan of care for lifespan and their families individuals with chronic dealing with chronic immune disorders. immune disorders. For each drug classification, students must understand the following details based on Sealock & Seneviratne et al. (2021/2024) Generic Name/Trade Names Classification Indications Mechanism Of Action Student  pharmacokinetics – absorption, distribution, metabolism & excretion, half-life, Preparati onset/peak/duration) Contraindications/Precautions Adverse Reactions/Side Effects on  toxicity and management of overdose Interactions (drug-drug, food-drug) Route/Dosage Nursing Considerations  Lab values/assessment and monitoring priorities Nursing interventions Patient and Family Teaching Additional  Self Study: Human Immunodeficiency Virus (HIV) Immune System: Defense 1st line Skin, mucous membranes, enzymes, natural of def microbial flora Innate ens Immunity 2end line of Phagocytes (granulocytes, macrophages) def ens 3erd Adaptive line of Lymphocytes: T-cells, B-cells Immunity def ens e T Cells: B Cells: Central to Produce immune antibodies and activation and contribute to cytokine autoimmune Immune production. responses. System: Key Players Antibodies: Bind to Macrophages : Process pathogens or antigens, self-antigens secrete to neutralize or cytokines, and flag them for initiate destruction. inflammation. Cytokines: Immune Regulation What are Cytokines? Small proteins that act as messengers between immune cells. Key role in coordinating and regulating immune responses (inflammation, immune activation, and suppression). Type of Function Examples Examples of Drug Classes Cytokine Pro- Drive inflammation and activate the TNF-alpha, IL-1, TNF inhibitors (e.g., infliximab, inflammatory immune system IL-6 adalimumab); IL-6 inhibitors (e.g., Cytokines tocilizumab) Anti- Suppress inflammation and promote IL-10, TGF-beta Modulated indirectly by inflammatory immune regulation interferons (e.g., interferon-beta) Cytokines Growth and Stimulate the growth, activation, and IL-2, IL-4, IL-7 JAK inhibitors (e.g., baricitinib, Differentiatio survival of T cells, B cells, and natural tofacitinib) n Cytokines killer cells Interferons Enhance antiviral defenses and IFN-alpha, IFN- Interferons (e.g., interferon-beta modulate immune activity beta, IFN- for MS) gamma Chemokines Guide immune cells to infection or CXCL8 (IL-8), No direct drug classes, but injury sites CCL important for immune cell migration Prior to Tuberculosis beginning any Hepatitis C and B medication that Any acute (pneumonia) or suppresses the chronic infection (osteomyelitis) immune Vaccination status system, patients are Pregnancy status and potential typically considerations for future screened for... reproduction Immune Modifying Therapy Nursing Implications Review of Agency Policies Regarding Administration of Immune Modifying Therapy It is essential to review the medication administration protocols of the University of Calgary and Alberta Health Services concerning who is permitted to administer immunosuppressants and the requirements for an independent double-check. Individual units may have their own specific safeguards. For example, at Foothills Medical Centre (FMC), Unit 37 does not allow nursing students to work with transplant patients. Safe Handling and Safe Disposal of Cytotoxic Medications Immune Modifying Therapies Immunosuppressants: Dru gs that reduce immune system activity (e.g., corticosteroids, calcineurin inhibitors). Immunomodulators: Drug s that regulate or enhance immune responses without broadly suppressing them (e.g., interferons, IVIG). Immune Modifying Therapies Category Medication Class Broad Immunosuppressant Corticosteroids Targeted Immune Calcineurin and mTOR inhibitors Suppressants Cytotoxic and Mycophenolate, JAK inhibitors Antiproliferative Agents Antibody-Based Therapies Monoclonal and polyclonal antibodies Immune Modulators Interferons, interleukin inhibitors, IVIG *DMARDs Nonbiologic and biologic Immune Modifying Therapy General Nursing Lab CBC & Differential Considerations s C-reactive Protein (CRP) Head-to-Toe Assessment Considerations Allergy Liver Function Infection Hypertension Bleeding Kidney Function Toxicity: liver, kidney, or lung Side effects associated with inhibiting cell division Chest radiograph (CXR) As part of the “right assessment.”  Confirm the last dose time to prevent pharmacokinetic Serum drug levels disruption  Confirm the last dose time to prevent pharmacokinetic disruption  Always safeguard against potential drug/drug and/or drug/food interactions. Examples: Prednisone, Dexamethasone, Methylprednisolone. Indications: Short-term management of acute immune flares (e.g., lupus, RA). Adjunct in transplant rejection prevention. Used in combination with other immunosuppressives for long-term disease control. Corticosteroids like prednisone are frequently Corticostero used as adjuncts to DMARD therapy during acute flares of rheumatoid arthritis or lupus ids: Review Mechanism of Action: Reduce inflammation by inhibiting phospholipase A2, decreasing prostaglandin and leukotriene synthesis. Suppress immune response by reducing cytokine production and lymphocyte proliferation. Adverse Effects: Long-term use: Osteoporosis, hyperglycemia, hypertension, adrenal suppression, Cushing’s syndrome. Short-term use: Mood changes, fluid retention. Glucocorticoids cannot be abruptly stopped. Examples: Cyclosporine, Tacrolimus Indications: Prevention of organ transplant rejection. Treatment of autoimmune diseases Calcineurin such as rheumatoid arthritis and psoriasis. Inhibitors Mechanism of Action: block calcineurin, a protein needed for activating T-cells and producing interleukin-2, which are essential for cellular proliferation; thereby suppressing the immune system. Adverse Effects: Nephrotoxicity Hypertension Hyperkalemia Neurological effects (e.g., tremors, headaches) Calcineurin Increased risk of infections Inhibitors Drug Interactions: Grapefruit juice (increases drug levels by inhibiting CYP3A4). NSAIDs (increased risk of kidney damage). Phenytoin, rifampin (reduce drug efficacy by increasing metabolism). Examples: Sirolimus (Rapamune), Everolimus (Zortress) Indications: Organ transplant rejection prevention. Treatment of specific cancers (e.g., renal cell carcinoma). Mechanism of Action: mTOR inhibitors block mTOR, a protein that controls T-cell growth and division after being activated mTOR by interleukin-2. By interrupting this process these drugs suppress the immune Inhibitors system. Adverse Effects: Hyperlipidemia, thrombocytopenia, delayed wound healing Drug Interactions: CYP3A4 inhibitors (e.g., ketoconazole) increase drug levels. CYP3A4 inducers (e.g., rifampin) decrease efficacy. Examples: Methotrexate, Azathioprine, Mycophenolate mofetil Indications: Lupus nephritis Autoimmune hepatitis Rheumatoid Arthritis Cytotoxic Organ transplant maintenance therapy (Antiprolifera tive) Agents Mechanism of Action: Antiproliferative drugs work by blocking DNA or RNA synthesis (through different pathways), preventing rapidly dividing immune cells like T and B lymphocytes from growing and functioning. This suppresses the immune system, making these drugs effective for treating autoimmune diseases and preventing transplant rejection. Adverse Effects: Bone marrow suppression (anemia, leukopenia, thrombocytopenia) GI disturbances (nausea, vomiting, diarrhea) Cytotoxic Hepatotoxicity (Antiprolifera Increased infection risk tive) Agents Drug Interactions: Allopurinol (increases azathioprine toxicity). Antacids and cholestyramine (reduce absorption of mycophenolate). Examples: Tofacitinib, Baricitinib Indications: Rheumatoid arthritis, Psoriatic arthritis, Ulcerative colitis Mechanism of Action: block Janus kinase Cytotoxic (JAK) pathways, which are crucial for transmitting signals from cytokines that (Antiprolifera activate the immune system. By disrupting this signaling, they reduce inflammation and tive) Agents: immune overactivity, making them effective for autoimmune diseases. Janus Kinase Adverse Effects: Increased risk of (JAK) Inhibitors infections, elevated liver enzymes, thrombosis Drug Interactions: CYP3A4 inhibitors/inducers can alter drug metabolism. Examples: Infliximab (Remicade), Rituximab (Rituxan), Adalimumab (Humira) Indications: Rheumatoid arthritis Crohn’s disease and ulcerative colitis Psoriatic arthritis Multiple sclerosis Monoclonal Mechanism of Action: Antibodies Infliximab/Adalimumab: TNF-alpha inhibitors block tumour necrosis factor- alpha (TNF-alpha), a key inflammatory cytokine, to reduce inflammation and immune system overactivity. Rituximab: Targets CD20, a protein on B lymphocytes, marking them for destruction. This reduces B cell-driven immune responses Adverse Effects: Infusion-related reactions (fever, chills, rash) Increased risk of infections Monoclonal Drug Interactions: Antibodies Live vaccines (contraindicated during therapy). Concurrent immunosuppressive drugs (increases risk of severe infections). Example: Anti-Thymocyte Globulin (ATG) (Thymoglobulin, Atgam) Indications: Prevention and treatment of acute organ transplant rejection. Aplastic anemia unresponsive to other therapies. Mechanism of Action: made from animals (rabbits or horses) immunized with human T cells, these antibodies target multiple T-cell antigens. They bind to T cells, leading to their destruction by the immune system. This suppresses the immune response and is used to treat transplant rejection or Polyclonal severe autoimmune diseases Adverse Effects: Antibodies Infusion reactions (e.g., fever, chills, hypotension) Risk of infection due to immunosuppression Serum sickness (delayed hypersensitivity reaction). Drug Interactions: Immunosuppressants (e.g., calcineurin inhibitors): Additive immunosuppressive effects increase infection risk. Live vaccines: Contraindicated during therapy due to immunosuppression. BC Transplant: Medication Guidelines Examples: Interferon beta-1a (Avonex, Rebif), Interferon beta-1b (Betaseron). Indications: Multiple Sclerosis (MS): Reduces relapse rates in relapsing- remitting MS. Mechanism of Action: : Interferon beta reduces inflammation by altering cytokine production. It decreases the levels of pro- inflammatory cytokines while increasing the levels of anti-inflammatory cytokines. This shift calms the overactive immune system, which Interferons helps reduce the damage to myelin in Multiple Sclerosis (MS). By controlling inflammation, interferons play a role in slowing the progression of MS and reducing the frequency of relapses. Adverse Effects: Flu-like symptoms, injection site reactions, depression. Drug Interactions: Immunosuppressants: Increased risk of infections. Hepatotoxic drugs: Additive liver toxicity. Treatments for MS Examples: Tocilizumab (Actemra), Secukinumab (Cosentyx), Ustekinumab (Stelara). Indications: Rheumatoid arthritis (Tocilizumab). Psoriatic arthritis, ankylosing spondylitis (Secukinumab). Crohn’s disease, psoriasis (Ustekinumab). Mechanism of Action: Blocks specific interleukin pathways to reduce inflammation and immune Interleukin activation. Adverse Effects: Inhibitors Increased infection risk. Injection site reactions. Drug Interactions: Avoid live vaccines during therapy. Immunosuppressants: Additive effects increase infection risk. Canadian Association for Psoriasis Patients: Treatment Arthritis Society Canada: Tocilizumab Crohn’s and Colitis of Canada: Biologics Examples: Gammagard, Privigen. Indications: Immune thrombocytopenia (ITP). Kawasaki disease. Primary immunodeficiencies. Intravenous Mechanism of Action: Provides passive immunity. Immunoglob Modulates immune responses by neutralizing ulin (IVIG): autoantibodies and inflammatory cytokines. Review Adverse Effects: Infusion reactions, headache, thromboembolism. Drug Interactions: Avoid live vaccines within 6 months of IVIG therapy. Canadian Blood Services: Immunoglobulin Products Medications that slow or halt the progression of autoimmune diseases, particularly rheumatic disorders. Indication: Reduce inflammation, prevent joint damage, and improve long-term outcomes. Disease Categories: Non-Biologic DMARDs: Synthetic Modifying compounds that broadly suppress the Antirheuma immune system. Examples: Methotrexate, Sulfasalazine, tic Drugs Leflunomide, Hydroxychloroquine. Biologic DMARDs: Targeted therapies that (DMARDs) interfere with specific immune pathways. Examples: infliximab, adalimumab Many DMARDs are used beyond rheumatic diseases (e.g., IBD, psoriasis, and transplant rejection). Arthritis Society Canada: Medication Reference Guide: Non Biologic Arthritis Society Canada: Medication Reference Guide: Biol ogic Methotrexate: Inhibits dihydrofolate reductase, reducing DNA synthesis and T-cell activation. Indications: Rheumatoid arthritis, psoriasis, and some cancers. Adverse Effects: Bone marrow suppression, hepatotoxicity, stomatitis. Drug Interactions: NSAIDs, TMP-SMX, Nonbiologic PPIs, Aspirin/Salicylates, Folic Acid/Folinic Acid, Penicillins, Alcohol, Leflunomide, Live DMARDs Vaccines Sulfasalazine: Reduces inflammation by modulating immune pathways. Indications: Rheumatoid arthritis, ulcerative colitis. Adverse Effects: GI disturbances, hypersensitivity reactions. Drug Interactions: Folic Acid, Methotrexate, Antibiotics, Warfarin Hydroxychloroquine: interferes with how macrophages process antigens, reducing their ability to activate T cells. Indications: Rheumatoid arthritis, lupus. Adverse Effects: Retinopathy (requires regular eye exams). Drug Interactions: Tamoxifen, Digoxin, Antacids Leflunomide (Arava): blocks pyrimidine Nonbiologic synthesis, which is essential for DNA production in rapidly dividing cells like DMARDs lymphocytes. This slows lymphocyte proliferation, reducing immune system activity. Indications: Rheumatoid arthritis. Adverse Effects: Hepatotoxicity, hypertension, gastrointestinal disturbances. Drug Interactions: Warfarin (increased bleeding risk); other hepatotoxic drugs. Infliximab (Remicade) Indications: Rheumatoid arthritis, Crohn’s disease, psoriasis. Adverse Effects: Infusion reactions, infections (e.g., TB). Adalimumab (Humira) Indications: Rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, IBD. Adverse Effects: Infections, injection site reactions, Biologic increased risk of malignancies. Rituximab (Rituxan) DMARDs Target: CD20 on B lymphocytes. Indications: Rheumatoid arthritis (refractory), lupus, certain cancers. Adverse Effects: Infusion reactions, hepatitis B reactivation, hypogammaglobulinemia. Etanercept (Enbrel) Indications: Rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis. Adverse Effects: Injection site reactions, increased risk of infections. Chronic Immune Disorders Chronic autoimmune disorder causing inflammation of synovial joints. Affects multiple systems if untreated, leading to joint deformity and disability. DMARDs (non- biologic and biologic) are foundational treatments; nursing management is critical for monitoring side effects and maintaining function. Treatment Self management: low intensity, low impact exercise to Rheumato combat joint stiffness, healthy diet, physiotherapy and occupational therapy id Medication Management Non-Biologic DMARDs: Arthritis Most common: Methotrexate (cornerstone therapy) with folic acid (RA) Sometimes: Sulfasalazine, Hydroxychloroquine, Leflunomide; Often used in combination. Biologic DMARDs: TNF-alpha inhibitors (e.g., infliximab, adalimumab). IL-6 inhibitors (e.g., tocilizumab) for refractory cases. Corticosteroids: Short-term use for acute flares. NSAIDs: Used in patients to promote physical comfort. Monitor patients for GI and renal effects Interprofessional Collaboration, Nursing Management and Patient Teaching Physiotherapy helps maintain joint motion and muscle strength Occupational therapy helps to develop upper extremity function and encourages joint protection Rheumato through the use of splints or other devices Suggest strategies for activity pacing id A caring, long-term relationship with RA healthcare team and/or support group can promote a patient’s Arthritis self-esteem and positive coping. Encourage patients considering complementary (RA) therapies like massage therapy, naturopathic medicine, special herbs, supplements, acupuncture, and meditation to discuss these with their MRHP. A dietitian can provide personalized education based on the patient's context, such as the risk of osteoporosis from corticosteroid therapy or changes in appetite that may lead to weight gain or loss, or underlying disease processes. Nursing Management and Patient Teaching Collaborate with the team and the patient to develop an action plan and coping strategies to Rheumato manage: Fatigue id Pain Arthritis Depression Limited endurance and mobility deficits (RA) Prevent exacerbations Age-related considerations Drug Therapy for JIA: NSAIDS are first line agents: ibuprofen, naproxen Non-Biologic DMARDs: methotrexate Corticosteroids Juvenile Biologic DMARDs: effective in this population, with ongoing studies regarding long-term use Idiopathi Physiotherapy is individualized for each patient and specific to each joint, strengthen muscles, c mobilize restricted joint motion, and prevent or correct deformities Arthritis Occupational therapy assumes the role for generalized mobility and ADL Relieve pain Pharmacologically (opioids are only short-term) and non-pharmacological modalities Multisystem autoimmune disorder characterized by periods of flares and remission. Common symptoms: fatigue, joint pain, skin rashes (e.g., butterfly rash), kidney involvement (lupus nephritis). First-Line Therapy: Nonbiologic DMARDs: Hydroxychloroquine Systemic Reduces disease flares. Lupus Adjuvant Therapies Corticosteroids: For acute flares and organ- Erythemato threatening disease. sus (SLE) NSAIDs: Used in patients with mild polyarthralgia or polyarthritis. Monitor patients for GI and renal effects. Cytotoxic Agents: methotrexate, azathioprine, Mycophenolate mofetil, cyclophosphamide. Biologic DMARDs: Belimumab for refractory cases. Nursing Management and Patient Teaching: Educate patients on sun protection to prevent flares. Monitor for signs of kidney involvement (e.g., proteinuria, edema). Systemic Teach infection prevention strategies due to Lupus immunosuppressive therapy. Erythemato Address psychosocial support needs (e.g., sus (SLE) fatigue management, mental health resources). Patients on Hydroxychloroquine can experience retinal toxicity -> retinopathy. All patients must have complete baseline ophthalmologic exams and regular follow - up exams annually (or as directed by MRHP) Lifelong immunosuppressive therapy required to prevent graft rejection. Common organs: kidney, liver, heart, lung. Calcineurin Inhibitors: Tacrolimus, Cyclosporine (cornerstones for rejection prevention). Transplant mTOR Inhibitors: Sirolimus, Everolimus for adjunct therapy. Corticosteroids: Prednisone for early post-transplantation and flare management. Polyclonal Antibodies: Anti- thymocyte globulin for acute rejection. BC Transplant: Medication Guidelines Nursing Management Monitor for rejection symptoms: fever, graft dysfunction (e.g., creatinine elevation in kidney transplant). Assess for medication side effects: Nephrotoxicity with calcineurin inhibitors. Transplant Hyperlipidemia with mTOR inhibitors. Therapeutic level monitoring for calcineurin and mTOR inhibitors. Provide infection prevention education: hand hygiene and avoiding crowds. Coordinate care with the multidisciplinary team (e.g., dietitian, pharmacist). Immune Deficiency SCID is a rare, life-threatening condition characterized by severe defects in both T-cell and B- cell function, leading to profound immune deficiency. Treatment for SCID is HSCT from a histocompatible donor, a haploidentical donor (usually a parent), or a matched unrelated donor. Severe IVIG infusions and Pneumocycstitis jiroveci Combined pneumonia (PJP) prophylaxis are used to augment the humoral immunity until the transplant is Immunodeficie performed. ncy (SCID) Nursing care focuses on preventing infection and supporting the child and family Prognosis for SCID is very poor if a compatible bone marrow donor is not available, nursing care is directed at supporting the family in caring for a child with a life-threatening illness Genetic counselling is essential because of the modes of transmission in either form of the disorder Resources Lupus Society of Alberta - https://lupus.ab.ca/ Lupus Canada- https://www.lupuscanada.org/ Lupus Foundation of America- https://www.lupus.org/ Alberta Rheumatology - https://albertarheumatology.com/ Rheumatoid Arthritis Society of Canada- https://arthritis.ca/about-arthritis/arthritis-types-(a-z)/ty pes/rheumatoid-arthritis

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