Nurs497Week1ImmunologySTUDENT-SN PDF

Introduction to course: Immunology SLIDES BY SARAH NIXON RN MN PRESENTATION ADAPTED FROM SLIDES BY KIMBERLY HELLMER MN RN/ KARA SEALOCK EDD MED BN RN CNCC (C) CCNE AND LEAH TELLIER MN RN JANUARY 14, 2025 Topics for today and Objectives: Human Immunodeficiency Virus (HIV) Acquired Immune Defici...

Introduction to course: Immunology SLIDES BY SARAH NIXON RN MN PRESENTATION ADAPTED FROM SLIDES BY KIMBERLY HELLMER MN RN/ KARA SEALOCK EDD MED BN RN CNCC (C) CCNE AND LEAH TELLIER MN RN JANUARY 14, 2025 Topics for today and Objectives: Human Immunodeficiency Virus (HIV) Acquired Immune Deficiency Syndrome (AIDS) Systemic Lupus Erythrematosus (SLE) Rheumatoid Arthritis (RA) Juvenile Idiopathic Arthritis Severe Combined Immunodeficiency (SCID)- Pediatric Conditions Long Covid Objectives: Reflect on Anatomy and Physiology of Immune system and look at how it relates to chronic illness Explain pathophysiology of the above conditions Examine relevant nursing assessments, clinical manifestations, and relevant lab values related to various conditions Human Deficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS) What/Why (Etiology-Risk factors)/Where (Epidemiology)? Why- WHO estimates that at end of 2019- 38 million people were living with HIV/Aids worldwide What- A virus that infects and destroys CD4-positive (CD4+) T-helper cells (Th cells)- Lymphocyte -Other Cd4+ cells- Monocytes, macrophages, astrocytes, oligodendrocytes Why is that bad- because Th cells activate B cells and Killer T cells in response to an invader Reminder- All viruses require host cell to reproduce Theres more- HIV is a retrovirus, what does this mean?  Blood born pathogen- Transmission through: Blood or blood products IV med use Etiology Heterosexual and homosexual activity Maternal-child transmission before or during birth (low risk in breast milk)  Ways HIV is NOT transmitted By mosquitoes, ticks, or other insects Through saliva, tears, or sweat Hugging, shaking hands, sharing toilets, sharing dishes, or closed-mouth or social kissing with someone who has HIV Through sexual activities that don’t involve the exchange of body fluidshttps://www.cdc.gov/hiv/basics/hiv-transmission/not- transmitted.html Through the air Figure 8-8 , p. 198, Power-Kean et al., (2023) HIV Pathophysiology Initial Viremia (high viral load- see peak blue wave) Latency period- 2-12 years Eventually, however, the ability of HIV to destroy CD4+ Th cells exceeds the body’s ability to replace the cells. The result is a decline in the CD4+ Th-cell count and a decrease in immune capability.​ Severe health problems develop with fewer than 200 CD4+ T cells per cubic millimetre (AIDS) Figure 8-9, p. 200, Power-Kean et al., (2023)​ Clinical Manifestations- HIV to AIDS 1. Early Symptoms non specific to HIV are (acute seroconversion):​ Fatigue, fever, muscle aches and headaches​ HIV multiplies and destroys CD4 cells; body producing HIV antibodies​ HIV level [viral load] high; risk of HIV transmission high​ 2. Early stages of HIV disease are usually asymptomatic to lymphadenopathy (latency/asymptomatic or chronic HIV infection)​ Viral load increases and CD4 cells progressively decrease​ 3. Acquired Immunodeficiency Syndrome (AIDS)- most severe phase​ HIV level [viral load] high; risk of transmission high​ CD4 cells low; risk of opportunistic infections high​ Poor Prognosis https://hivinfo.nih.gov/understanding-hiv/fact- sheets/stages-hiv-infection Diagnostic Tests Three Main Types of HIV Tests: Nucleic acid tests (NATs)  Check blood for presence of the virus’ RNA  Determine how much virus present [viral load] Antibody and antigen tests  Test for presence of HIV antibodies and antigens  HIV produces antigen p24 [before body starts producing antibodies to HIV] Antibody tests  Test for HIV antibodies  Venous blood better for detection  Can use oral fluid or finger prick blood-later detection [basis of home-testing kits] Typical AIDS Progression Asymptomatic Seronegative Status Asymptomatic Seropositive Status Subclinical immune deficiency Lymphadenopathy (early AIDS) AIDS related complex (middle stage with combination of symptoms) AID S Clinical Manifestations- AIDS Fatigue​ Unexplained weight loss: greater than 10%​ Fever​ Lymphadenopathy​ Skin or mucous membrane lesions: purplish-red nodules Cough​ Persistent diarrhea​ Tongue/mouth “thrush”​ Perianal vesicular and ulcerative lesions of herpes simplex infection​ AIDS related cancer-Kaposi’s sarcoma​ Cytomegalovirus retinitis  Opportunistic Infections  Fungal Infections: Bacterial Infections Other Infections  Candidiasis (YEAST)  Mycobacterium avium complex (MAC)  Cellulitis (esophageal, tracheal, or  Mycobacterium Tuberculosis  Osteomyelitis pulmonary, vulvovaginal) (disseminated or extrapulmonary)  Endocarditis  Cryptococcus (CNS infection)  Nocardiosis (pneumonia, meningitis,  Varicella zoster virus disseminated)  Coccidioidomycosis  Salmonella infections (septicemia, (disseminated) recurrent)  Histoplasmosis (disseminated) Cancers Viral Infections  Kaposi's sarcoma  Protozoal Infections  Cytomegalovirus (CMV) (pulmonary,  Invasive uterine/cervical  Cryptosporidiosis or isosporiasis intestinal, retinitis, or CNS) cancer (enteritis)  Herpes simplex (Iocalized or  Non-Hodgkin's  Pneumocystosis (pneumonia or disseminated) Lymphomas (Burkitt, disseminated infection)  Progressive multifocal immunoblastic)  Toxoplasmosis (pneumonia or leukoencephalopathy (PML)  Primary lymphoma of CNS infection) the brain  HIV and AIDS Nursing Assessment  Nursing Assessment for HIV: Nursing Assessment for AIDS:  NEURO:  NEURO: confusion, memory, HAND  CV: (cognitive, motor, behavioral), meningitis,  RESP: dementia No major  CV: endocarditis changes  GI:  RESP: pneumonia, candidiasis  GU:  GI: enteritis  INTEG:  GU: vulvovaginal candidiasis,  Health History: at risk uterine/cervical cancers populations or unprotected  INTEG: Kaposi's sarcoma, herpes simplex, intercourse with a positive person cellulitis, herpes zoster not on ART or in a undetectable = untransmissible state  LABS: HIV positive + clinical symptoms of opportunistic infections, CD4 cell count,  LABS: HIV positive labs associated with above conditions Photos  Considerations for Birth Parents who are Living with HIV Obstetrical complications increased risk for:  Increased risk for preterm labour and birth  premature rupture of membranes  perinatal loss  or Intrauterine growth restriction (IUGR) Post partum Complications increased risk for:  Postpartum UTIs  Vaginitis  Post partum endometritis  Poor wound healing  HIV-related thrombocytopenia may also increase the risk for hemorrhage  Neonatal/Pediatric AIDS Neonatal AIDs transmission may be placental, contact with maternal blood at birth, or postnatal exposure to parent who is infected (i.e. breastfeeding). Classic signs evident in adult often not present. Increased risk for developing non-Hodgkin lymphoma and Kaposi sarcoma. Common signs:  Developmental  Oral candidiasis delay  Bacterial infections  Parotitis  Failure to thrive  Lymphadenopathy (swollen lymph nodes)  Hepatosplenomegaly  Chronic or recurrent diarrhea Autoimmune Disorders SLE- SYSTEMIC LUPUS ERYTHEMATOUS RA- RHEUMATOID ARTHRITIS Systemic Lupus Erythematosus (SLE) What/Why (Etiology-Risk factors)/Where (Epidemiology)? SLE is an autoimmune disease - 1 in 2000 Canadians - Most common in women in the 20-40 age range and black individuals have eightfold increased risk Etiology: A chronic, inflammatory, connective tissue disease of unknown origin. Multifactorial origin resulting from interactions among genetic, hormonal, environmental, and immunological factors. Unique Factors- Triggers: UV light, estrogen, infections, medications More of the What Osmosis video pic  Clinical Manifestations Most commonly affected tissue is: General Clinical Manifestations:  Arthralgia or arthritis (90% of Fever individuals)  Vasculitis (blood vessels) and rash Weight loss (70-80% of individuals) Arthralgia  Renal disease (40-50% of individuals) Excessive fatigue  Hematological abnormalities (50% of individuals with anemia being most common complication)  Cardiovascular diseases (30-50% of individuals)  Photophobia Fig 69.9, pg. 1686, Tyerman & Cobbett, (2023)  Dermatological Manifestations Butterfly (Malar) vs Discoid Rash https://www.sciencedirect.com/science/ https://www.sciencedirect.com/topics/medicine-and- article/abs/pii/B978070206896600051X dentistry/malar-rash https://standardofcare.com/discoid- lupus/  Notable Manifestations- MSK -Swan neck appearance in joints Ulnar deviation (towards ulna- “L”ittle finger) https://www.sciencedirect.com/science/article/abs/pii/ S1521694209000448 Cardio Renal Lupus nephritis​ Inflammatory complication​ Tachypnea and cough suggest restrictive lung Complexes of autoantibodies and disease​ Pleurisy with or without pleural effusions​ complement accumulate in the glomerulus, causing cell proliferation, Dysrhythmiasà fibrosis of the SA and AV nodes inflammation, and injury​ Hypertension and hypercholesteremia​ Clinical manifestations include:​ Edema​ Proteinuria, edema and signs of nephrotic syndrome (hypoalbuminemia, Antiphospholipid syndrome ​ hypolipidemia, lipiduria, decreased Pericarditis vitamin D levels, hypothyroidism)​ Disease progression may be silent or may progress to end-stage kidney failure https://knowmedge.com/blog/medical-mnemonics-diagnostic-criteria-for-sle- soap-brain-md/  Diagnosing SLE: Criteria Explanation Laboratory Tests: Pericarditis, pleurisy on electrocardiogram or ANA (antinuclear Serositis imaging scan antibody) Oral ulcers Sores, usually painless, on the lips and in the anti-DNA antibody mouth complement levels Nonerosive arthritis-tenderness or swelling of Arthritis two or more peripheral joints anti–double-stranded DNA Unusual skin reaction (skin rash) to sun antibody assay Photosensitivity exposure Leukopenia, lymphopenia, thrombocytopenia, Complete blood count(CBC) Blood disorder hemolytic anemia erythrocyte sedimentation Renal involvement Proteinuria, cellular casts rate(ESR)- RBCs Antinuclear Urinalysis(UA) Elevated titers antibodies blood urea nitrogen(Urea or Immune Presence of antibodies or lupus erythematosus BUN) phenomenon cells creatinine(Cr) Neurological Seizures or psychosis in absence of other disorder causes creatine kinase(CK) liver function tests(LFTs: LD, Malar rash Fixed erythema over cheeks and nose ALT, AST, ALP, GGT, Raised, red lesions with scaling and follicular Discoid rash plugging Bilirubin, Albumin)  SLE Nursing Assessment  Nursing Assessment:  NEURO: seizures, cognitive dysfunction, strokes, meningitis, headache  CV: dysrhythmias, HTN, hypercholesteremia, edema, antiphospholipid syndrome, pericarditis  RESP: tachypnea with cough, pleurisy with or without pleural effusions  GI: abdominal pain  GU: lupus nephritis, end-stage kidney failure  INTG: malar rash, alopecia, discoid erythema, urticaria, purpura, petechiae, leg ulcers  MSK: polyarthralgia, morning joint stiffness, arthritis  LABS: CBC, ANA, electrolytes, magnesium, TNT, coagulation, CRP Rheumatoid Arthritis  What- chronic, systemic, inflammatory autoimmune disorder distinguished by joint swelling and tenderness and destruction of synovial joints Usually affects joints symmetrically What/Why Frequent- wrists, hands, elbows, (Etiology-Risk shoulders, knees, and ankles factors)/Where Characterized by dysregulated (Epidemiology)? inflammatory processes in the synovium of the joint, leading to eventual destruction of cartilaginous and bony elements of the joint, resulting in pain and disability​ Etiology- Genetic and Environmental Triggers​ Patho described Inflammatory process Citrullinated proteins (seen as Antigens) Autoantibodies (Immunoglobulins) known as RF (Rheumatoid factor) form RF binds with antigens form Immune complexes T and B lymphocytes activated Increased RF and enzymes Increased Inflammatory response (Vicious cycle) RA Pathophysiology Pannus  Pannus (highly vascular granulation tissue)  Covers and erodes entire surface of the articular cartilage  Damage eventually causes joint laxity, subluxation and contracture Figure 39.19, p. 986, Power-Kean et al. (2023) Fig 39-20, p. 987, Power-Kean et al. (2023) Clinical Manifestations of RA Deformities of Chronic Advanced RA  Swan Neck and Boutonniere http://stanfordmedicine25.stanford.edu/the25/ hand.html https://www.physio-pedia.com/ Hand_Rheumatoid_Arthritis Complications of Rheumatoid Arthritis  Joint destruction Nodules on vocal chords  Flexion contractures Carpal tunnel syndrome  Hand deformities- Cardiac complications difficulty grasping Pulmonary complications  Nodular myositis Lymphadenopathy  Cataracts and glaucoma- Splenomegaly loss of vision  Rheumatoid Arthritis Nursing Assessment  Nursing Assessment:  NEURO: pain, fatigue (brain fog), weakness, fever  CV: anemia, thromboses (AMI, cerebrovascular occlusions), vasculitis  RESP: pleuritis, parenchymal nodules, pulmonary nodules and pneumoconiosis Caplan’s syndrome, diffuse pulmonary fibrosis  GI: anorexia, weight loss, mesenteric infarction (thromboses)  GU: kidney damage  MSK: pannus, joint stiffness, joint deformities  Skin: rashes, nodules  LABS: CBC, erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), anti- citrullinated protein antibody (ACPA), antinuclear antibody (ANA), C-reactive protein (CRP) https://www.youtube.com/watch?v=Fgk4T7Jat0w  Juvenile Idiopathic Arthritis (JIA)  A condition in which children under the age of 16 develop RA and experience swelling, tenderness, and pain in one or more joints and lymph nodes and splenic enlargement.  Arthritis present for at least 6 weeks before diagnosis (mandatory for diagnosis of JIA)  Three distinct modes of onset: 1.Oligoarthritis (fewer than 3 joints) 2. Polyarthritis (more than 3 joints) 3. Still disease (severe systemic onset) JIA Differs Large joints from RA Chronic uveitis (Uvea-middle layer of pigmented vascular structures of eye- pain, redness, blurry vision) Serum tests may be negative for Rheumatoid Factor Subluxation and ankyloses may occur in the cervical spine if disease progresses RA that continues through adolescence can have severe effects on growth and adult morbidity Clinical Manifestations: JIA Either insidious or abrupt disease onset, often with morning stiffness Complaints of joint pain (arthralgia) or abnormal joint use History of school absences or limited ability to participate in physical education classes Spiking fevers occurring once or twice each day- about the same time of day Evanescent rash on the trunk and extremities Psoriasis or more subtle dermatologic manifestations https://www.youtube.com/watch?v=E67Z6UER_Dc Severe Combined Immunodeficiency (SCID)  Epidemiology: Approximately 1 in 70 000 infants born in Canada are diagnosed with Severe Combined SCID. It is more common in Indigenous infants, with an estimated 1 in 20 000 births Immunodeficiency Etiology: (SCID) X-linked recessive that affects more males than females Combined deficiency that affects both T and B cells with little to no antibody production Pathophysiology: Few detectable lymphocytes in the circulation and secondary lymphoid organs Clinical Manifestations: Susceptibility to infections occurs most commonly in the first month of life Suffers from chronic infections and fails to completely recover from infections Failure To Thrive (FTT) is a consequence of persistent illnesses Nursing Assessment: Preventing infection and monitoring for signs and symptoms of new infections David Vetter – Bubble Boy born in 1971 with SCID lived in a “protective environment” his entire life (12 years) only treatment back then was bone marrow transplant by a direct match Think of how treatments have improved for SCID LONG COVID  Long COVID World Health Organization(WHO): Post COVID-19 condition Epidemiology: The Office for National Statistics in the UK estimated that the prevalence of symptoms remaining following 12 weeks ranged from 3% to 11.7%, with a substantial deleterious impact on social and professional life, and day-to-day activities Etiology: The evidence about what causes long COVID is still limited, and the underlying mechanisms thus remain ambiguous Antibodies against the ACE2 receptor have been identified in COVID-19 convalescent patients Key Descriptors: Presence of symptoms at least 2 months in individuals with a history of probable or confirmed SARS-COV-2 infection People can present symptoms following organ damage, while others may experience new symptoms in the aftermath of a mild infection  Long COVID Several mechanisms potentially involved in long COVID: Virus driven cellular alterations tending to attack or affect the nervous system preferentially Dysregulated immune system dysfunction i.e. Autoimmune manifestations, coagulation and fibrosis pathway activation, or metabolic disturbances Hypothesis of persistent and occult virus presence, based on the identification of viral particles in several organs after the acute infection Antibodies against the ACE2 receptor have been identified in COVID-19 convalescent patients. Which could lead to an increase in angiotensin II, and induce a proinflammatory state https://www.mountsinai.org/health-library/ diseases-conditions/long-covid  Long COVID: Clinical Manifestations System Signs & Symptoms Neurology Cognitive and mental health disorders Pain Headache Fatigue Anosmia/Agueusia Neuropathy Cardiovascular system Fatigue Dyspnoea Chest pain Respiratory Dyspnoea Chest pain Cough Long COVID: Clinical Manifestations System Signs & Symptoms Gastro-intestinal system No specific symptom-disrupted microbiome Immune system Remaining inflammation in blood samples analysis, long-lasting phenotypic and functional disorders of lymphocytes, decreased amounts of dendritic cells and persisting alterations Autoimmunity: auto-antibodies against the nociceptive receptors, immunomodulatory proteins and tissue components Persistence of the SARS-CoV-2 nucleic acids in tissues Multisystem Inflammatory syndrome in children (MIS-C) Dermatological system Skin Disorders  Long COVID Nursing Assessment  Nursing Assessment:  NEURO: A&Ox3, sleep disturbance, fatigue, headache, taste, smell, numbness & tingling, shooting nerve pain  CV: Fatigue at rest or with activity, shortness of breath, chest pain, diaphoresis, skin color, cap refill  RESP: Dyspnea, shortness of breath, tachypnea, chest pain, cough  GI: Abdominal pain, bloating, discomfort, changes in bowel habits  MSK: DVT risk factors-immobility, venous stasis, calf size, pulses, swelling and/or edema, pain to lower legs  Skin: any rashes or areas of irritation  LABS:CBC, Lytes, LFTs, Troponin, CRP, D-dimer  Lets Review: Key Points to Remember  Can you perform a full head to toe assessment with knowledge of physiological landmarks and anatomy and physiology related to Neuro, CV, Resp, GI and GU assessment pertaining to HIV/AIDS related illnesses, SLE and RA?  Explain the “why” associated with head-to-toe assessment and connections to other systems  Identify and apply concepts of lab values related to alterations in immunity  Do you understand the pathophysiology, clinical manifestations and nursing assessment related to:  HIV/AIDS related illnesses  SLE  RA  SCID  Long COVID The End- Welcome back to Patho