Immune System Study Guide PDF

Immune System: Types of Immunity: ● Acquired (adaptive): specific against a foreign antigen; result of prior exposure to an antigen; can be active or passive ● Active immunity: immunologic defenses developed by person’s own body; lasts many years; may last a lifetime ● Passive immunity: temporary, b...

Immune System: Types of Immunity: ● Acquired (adaptive): specific against a foreign antigen; result of prior exposure to an antigen; can be active or passive ● Active immunity: immunologic defenses developed by person’s own body; lasts many years; may last a lifetime ● Passive immunity: temporary, but protection is immediate; results from transfer of a source outside of the body that has developed immunity or introduction of antibodies from another person or animal ● EXAMPLES: ○ Receiving a varicella vaccine = artificial passive immunity ○ Having chicken pox as a child and not getting the disease later in life if exposed to it = active natural immunity ○ Giving an antigen immunoglobulin drug if a person was bitten by a snake = artificial passive immunity ○ Antibodies pass from mom to infant during breast feeding or pregnancy = active natural immunity ● Humoral vs Cellular Immunity: ○ Humoral immunity/B Lymphocytes involves the interaction between antigen and antibody, whereas Cell-mediated immunity/T cell lymphocyte occurs when T cells are required to search out foreign invaders and identify them for destruction Function of B and T cells, CD4 and CD8: ○ B cells: ■ Mature in bone marrow ■ Short lifespan ■ Antigen binds onto B cell receptor, which triggers the B cell to grow and clone itself into either plasma cells (generates antibodies and releases them into body binding to antigen signaling cells to kill the pathogen) or memory cells (help body mount a faster and stronger attack next time antigen invades) ○ T cells: ■ Required to search out foreign invaders and identify them for destruction ■ Differentiate in the thymus gland (small organ in upper chest gland that produces lymphocytes that fight off infections in the body); long lifespan ○ Helper T cells (CD4 glycoprotein): ■ Release cytokines (such as interferons and interleukins) that boost person immune system by signaling growth, differentiation and enhance the action of other immune cells like macrophages ■ Help B cells grow and develop antibodies more quickly ○ Cytotoxic T cells (CD8 cells): ■ Patrol the body looking for and can destroy pathogenic cells directly including cancerous cells Types of Antibodies/function: IGG, IGM, IGE ● IgM: body has a rise in this antibody FIRST (early infection response) ○ Can see levels right as person is infected and rises before IgG levels ○ Look at IgM to see if someone has recently been infected or if someone is still infected ○ Someone with active covid you can see IgM rise, which clears body quicker than IgG ● IgG: around 7-14 days depending on virus, you mount immunoglobulin G ○ Response is the later response and long lasting ○ To see if someone has long lasting immunity or mounted a long-lasting immune response ○ Starts spiking as IgM starts coming down ○ Shows us that someone has been infected and recovered from it Immunosuppressant: Cyclosporine ● Inhibits T cells ● Therapeutic uses: ○ Prevention of allogeneic organ transplant rejection ○ Prevention and treatment of graft vs host disease (GVHD) ○ Severe allergic reactions ● Adverse Effects: ○ Hirsutism ○ Gingival hyperplasia (expected) ○ Hyperlipidemia ○ HTN (BBW) ○ Nephrotoxicity (BBW) ○ Check WBC and platelet (report leukopenia WBC less than 4000) ○ Monitor for bleeding ○ No pregnant patients- use contraception ● BLACK BOX WARNING: ○ Increased risk of developing tumor (lymphomas) ○ Increased risk of developing skin cancer ○ Increased risk of solid organ tumors ● Interactions: ○ St. John.s wort decrease effects of cyclosporine ○ Carbamazepine, phenytoin, and rifampin decrease the effects of cyclosporine ● NOTE: ○ Therapeutic effects below normal therapeutic range can lead to organ rejection, which is why cyclosporine levels should be monitored Replication of HIV and Function of Reverse Transcriptase, Integrase, and Protease Enzymes: ● HIV replication ○ ○ ○ Called retroviruses because they replicate in a “backward” manner going from RNA to DNA Process in cells in which the enzyme makes a copy of DNA from RNA Newly formed double stranded DNA is infected w/ HIV because all genetic material is replicated during cell division ● Enzymes involved in HIV: ○ ○ ○ Reverse transcriptase: ■ makes DNA copy of viral RNA genome; as DNA is being formed reverse transcriptase degrades the RNA strand ■ Complementary DNA strand is then added by reverse transcriptase ● Double stranded DNA joined non-covalently ■ NRTI’s (zidovudine) adverse effects: ● Black box: granulocytopenia, aplastic, hemolytic anemia, pancytopenia ● Black box: lactic acidosis ● Black box: hepatomegaly with steatosis ● Black box: myopathy, myositis ● Other: fatigue, headache, n/v, anorexia ■ NNRTI’s (efavirenz) adverse effects: ● CNS effects (if develops, take at night): dizziness, insomnia, drowsiness, vivid dreams, depression ● Rash can be mild to severe desquamation-Steven Johnson syndrome ● Can also cause liver damage Integrase: ■ The double stranded viral DNA moves into host cell nucleus and inserted into the host cell chromosome by viral integrase enzyme ■ Inserts double stranded viral DNA into the host cell’s chromosome ■ The integrated viral DNA is now referred to as pro viral DNA ● RNA may be synthesized from DNA yielding messenger RNA and viral genome RNA ■ Integrase inhibitor (raltegravir) adverse effects: ● Headache, dizziness, n/v, diarrhea, fever, rhabdomyolysis ● Most common is elevated liver enzymes ● Elevated pancreatic enzymes ● Hyperglycemia Protease: ■ Enzyme involved in cutting and assembling process ■ Cleaves (cuts) the newly formed strands of HIV genetic material into smaller pieces ■ ■ ■ RNA may be synthesized from DNA yielding messenger RNA and viral genome RNA ● Viral messenger RNA is translated yielding viral enzymes and structural proteins Protease inhibitors (saquinavir mesylate) adverse effects: ● Back pain, fatigue, neuropathy, paresthesia, anxiety, depression, suicidal ideation ● Rash, eczema, pruritus ● Anemia, TTP, pancytopenia ● Hyperlipidemia ● Increased bleeding with pts with hemophilia ● Liver damage ● Decreased cardiac conduction-prolonged QT syndrome ● HTN, hypotension, chest pain Monitor K+ and mag levels in protease inhibitors and take within 2 hours of meal or on full stomach HIV: HIV fusion inhibitors (enfuvirtide) adverse effects: ● ● ● ● ● Fatigue, insomnia, nausea, diarrhea Injection site reactions Pneumonia Hypersensitivity reactions Assess CK for myalgia pain CCR5 Antagonist (maraviroc) adverse effects: ● ● ● ● ● ● ● ● ● Fever Rash URI Cough Dizziness, anxiety, depression Lipodystrophy Benign skin neoplasms, warts Conjunctivitis, otitis media Heptatotoxicity (Black box warning) Main goals of drug therapy: (HAART-highly active antiretroviral therapy) ● ● ● ● ● ● Decreased viral load Maintain/increase CD4+T counts Prevent HIV-related symptoms and opportunistic diseases Delay disease progression Prevent HIV transmission Reduce the plasma HIV RNA to its lowest possible level (HAART) Lab Monitoring for HIV and AIDS: ● ● ● CD4 count ○ Infection lowers the CD4 count (lower the count means the more weakened the immune system & predicts likelihood of opportunistic disease) ○ Normal count ranges from 800-1200 cells/mm3 ○ Count less than 200 cells/mm3 qualifies an AIDS diagnosis HIV viral load (best gauge of the level of HIV) ○ Low viral load=lower amount of HIV activity ○ Lowest levels of detectable viral load are about 40-75 copies/mL ○ Determined by measuring the amount of HIV RNA in the blood (this level is an estimate of how rapidly the virus is replicating) ○ Performed every 3-6 months to assess degree of effectiveness ○ GOAL is to reduce plasma HIV RNA to less than 75 copies CBC Tuberculosis: 2 questions- Review powerpoint slides only on INH and Rifampin Math Desirable Lab Ranges: ● ● ● ● ● ● ● ● Total serum cholesterol: less than 200 LDL: less than 130 HDL: 40 or above Triglycerides: less than 150 ○ Males: 40-160 mg/dL ○ Females: 35-135 mg/dL Creatine kinase (CK): 30-170 units/L ○ Detectable 3-6 hr following myocardial injury; present 2-3 days after Troponin T: less than 0.1 ng/mL ○ Detectable 2-3 hr following myocardial injury; present 10-14 days after Troponin I: less than 0.03 ng/mL ○ Detectable 2-3 hr; present 7-10 days after Myoglobin: less than 90 mcg/L ○ Detectable 2-3 hr following myocardial injury; present for only 24 hours For MI, make sure you know the difference between a NSTEMI and STEMI and how it affects pharmacological drug treatments and how they are treated. Know what an inverted T wave or inverted ST wave vs STEMI means and how it impacts treatment. Review labs used in diagnosing MI and priority nursing interventions. Difference between NSTEMI and STEMI: JC Core Measures for MI: ● AMI-1 aspirin at arrival ● AMI-2 aspirin prescribed at discharge ● AMI-3 ACEI or ARB for LVSD ● AMI-4 Adult smoking cessation advice/counseling ● AMI-5 beta blocker prescribed at discharge ● AMI-7 median time to fibrinolysis (alteplase) ● AMI-7a fibrinolytic therapy received within 30 minutes of hospital arrival ● AMI-8 median time to primary PCI ● AMI-8a primary PCI received ● AMI-10 statin prescribed at discharge Dysrhythmias: