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Complex Nursing 1

Immune/HIV/transplants/ABGs/respiratory

QuestionAnswer
Tonsils and adenoids (immune) prevents infections of the throat when you are young, but not very beneficial when older.
Where do T-cells mature Thymus
Where do B-cells mature Bone Marrow
Self-tolerance (immune) the ability of the immune system to distinguish host cells from foreign cells
3 types of T-cells T-helpers (activate B-cells), T-cytotoxic (phagocytosis), T-memory (acquired immune response for future infections)
2 types of B-cells B-plasma (produce antibodies to fight antigen), B-memory (acquired immune response for future infection)
NK cells Natural Killers. Part of the innate immune response. Non-specific phagocytosis.
Neutrophils Innate immune response; phagocytosis; first-responders to most infections
Eosinophils parasitic infections and allergy response
Basophils release chemotaxis to attract other WBC
Monocytes innate immune response, phagocytosis, and antigen presenting cell to activate T-cells.
Human Leukocyte Antigens cluster of 6 genetic markers used to identify which patients are good organ transplant matches
Stages of the innate immune response (non-specific response) 1. Vascular response: blood vessels constrict to stop bleeding, then dilate to allow excess fluid to enter area and causes inflammation 2. Cellular response: blood thickens WBC enter the area and begin phagocytosis 3. Tissue Repair and Resolution
Adaptive: Antibody Mediated (Specific response) B-cells come into contact with antigen and produce plasma and memory cells. Plasma cells produce antibodies to fight the antigen and memory cells create acquire immunity
Adaptive: Cell Mediated (Specific response) T-cells come into contact with sleeper cell antigens and produce cytotoxic cells, T-helpers, and memory cells. Cytotoxic cells destroy the sleeper cells, helper cells stimulate the production of more T and B cells, memory cells produce acquired immunity
Type 1 immunoglobulin (IgE) allergic reactions (peanut allergy), allergies (hay fever), anaphylaxis
Type 2 immunoglobulin (IgG/IgM) Cytotoxic response attacks self-cells that have foreign proteins attached to them. Examples: hemolytic anemia (RBC destroyed too early), transfusion reactions, good pastures syndrome (attacks collagen in kidneys and lungs), thrombocytopenic purpura
Type 3 immunoglobulin (IgG/IgM) trigger inflammation responses in kidneys, skin, joint, small vessels. Examples: rheumatoid arthritis, lupus, serum sickness
Type 4 immunoglobulin (T-cell mediated) Delayed hypersensitivity reactions. Examples: latex allergies, poison ivy, TB skin test
Types of Immunoglobulin immunoglobulin are antibodies that are produced by the B-plasma cells
Active Immunity acquired through the disease or vaccinations
Natural immunity acquired through getting the disease, placental, breast milk
Passive immunity passed through breast milk or placental/ injection of antibodies
Artificial Immunity passed through vaccinations
Anaphylaxis Histamines causes vasodilation and increased capillary permeability, third spacing of fluid, and hypovolemic shock.
Autograph transplant Transplant of your own tissues
Isograft transplant Transplant between identical twins
Allograft transplant Transplant between the same species
Xenograpft transplant Transplant between different species
HLA histocompatibility test Based on 6 genetic markers that determine transplant compatibility
Hyperacute tissue rejection Occurs immediately-3 days after transplantation. More likely in patients with past transplants. Organ will be become soft and cyanotic due to decreased blood perfusion (Triggered by pre-formed antibodies)
Acute tissue rejection Most common type. Occurs 4 day to 3 months after transplantation. Results in red and tenderness at site, fever, and organ failure. (Triggered by Cellular immune response)
Chronic tissue rejection Occurs 4 months to years after transplantation. Results in slow progressive organ failure. (Triggered by the Antibody mediated immune response)
Graft versus host disease Most commonly occurs with bone marrow transplant. Cell-mediated immune reaction where the body attacks its own host cells.
Symptoms of graft versus host disease Bright red rash on palms of hands and soles of feet, bloody diarrhea, and abdominal pain.
Acute GVHD Resolves within first 100 days
Chronic GVHD Resolves after 100 days
Pre-transplantation medications Antiviral and Antibiotic medications to prevent secondary infections
Post-transplantation medications Corticosteroids, T-cell suppressors, Cytotoxic agents, and antilymphocyte globulin
Corticosteroid considerations (post-transplant) Slow wound healing, hyperglycemia, mood changes, immune suppression, fluid retention
T-cell suppressing agent considerations (post-transplant) Monitor BUN/Creatinine levels. This drug is renal toxic
Cytotoxic Agent considerations (post-transplant) Monitor I&Os closely, risk for bleeding, and pulmonary fibrosis. This drug affects liver and kidneys
Antilymphocyte globulins considerations (post-transplant) Given via IV through a central line or port immediately after a transplant. Pre-treat with Tylenol and Benadryl to reduce risk of serum sickness
HIV virus attacks which cells CD4 T-cells
HIV is fought by which cells B-plasma antibodies
HIV Acute Retroviral Syndrome First 2-4 weeks after contracting HIV. Patient may present with flu-like symptoms and general malaise, but the viral antibodies are still undetectable by HIV tests
HIV diagnostic tests ELISA (fast and cheap), Western Blot (more specific), Viral load test (looks at CD4 counts and progression of the disease)
HIV Seroconversion Time at 5-6 weeks when the HIV antibodies are detectable by tests
Early Asymptomatic HIV infection Patient may be asymptomatic or have vague symptoms, middle interval before HIV symptoms appear. CD4 counts are still above 500.
Early Symptomatic HIV Infection Symptoms: herpes zoster, yeast infection, kaposis sarcoma, persistent lymphadenopathy (swollen lymph nodes)
Normal CD4 counts Greater than 500
CD4 count for AIDS diagnoses Less than 200 with opportunistic infections
What is the Ryan White Bill for HIV? A federal fund to help HIV patients pay for treatment
HIV Treatment: Transcriptase Inhibitors Interrupts DNA synthesis
HIV Treatment: Protease Inhibitors Blocks movement of HIV virus. Side effects include HTN, insulin resistance, obesity, and skeletal wasting
HIV Treatment: Reverse Transcriptase Inhibitors Interrupts RNA to DNA synthesis
HIV Treatment: Entry Inhibitors Blocks entry of HIV virus into healthy cells
HIV Treatment: HAART Therapy Combination anti-retroviral therapy that is highly active
Side effects of HIV HAART therapy Atrophy if fat and muscle stores in the body, insulin resistance, changes in extremities, muscle wasting, HTN, and hyperlipidemia
How do hypotonic fluids affect cells hypotonic fluids move fluid into the cells to make them bigger
How do hypertonic fluids affect cells Hypertonic fluids move fluid out of the cells to make them shrink
Symptoms of fluid deficit v blood pressure, ^ HR, v skin turgor, v urine output, edema
Symptoms of fluid excess ^ BP, ^ HR, ^ respiratory effort, crackles, edema, normal urine output, weight gain
Normal Sodium 135-145 (regulated by kidneys, helps control BP and muscle contraction)
Normal Potassium 3.5-5.0 (regulates cardiac contraction)
normal Calcium 8.5-10 (regulated by the parathyroid and dependent on albumin)
Normal Magnesium 1.6-2.6
normal Phosphate 2.5-4.5
Hyponatremia symptoms Na+ <135; muscle cramps, weakness, fatigue, N/V/D, headache, depression, lethargy, changes in reflexes, dulled senses, and irritability
Hypernatremia symptoms Na+ >145; extreme thirst, lethargy, weakness, irritability, seizures, coma, death. Flushing, restless, increased BP, edema, decreased urine output, low grade fever
Hypokalemia symptoms K+ <3. 5; confusion, depression, changes in nerve impulse transmission, respiratory arrest, muscle cramps, paralysis, fatigue, polyuria, polydipsia, severe heart arrhythmias (U wave with ^ risk of V-tach/V-fib)
Treating hypokalemia Administer oral or IV potassium chloride with magnesium (Mg helps with K+ absorption)
Hyperkalemia symptoms Muscle cramps, bradycardia, weakness, tremors, peaked T-wave with widening QRS complex which can lead to CARDIAC STANDSTILL
Treating hyperkalemia Kayexalate enema/oral K+ laxative, insulin/glucose tx, hemodialysis, stop K+ supple
Hypocalcemia symptoms Tetany (muscle stuck), Chvostek's sign (cheek twitching), Trousseau's sign (BP cuff causes arm to contract), lung stridor, convulsion, seizures
Tetany Muscle stuck in contraction (r/t hypocalcemia)
Chvostek's sign Cheek muscles twitch when flicked (r/t hypokalemia)
Hypercalcemia symptoms Weakness, fatigue, kidney stones, cardiac arrest, confusion, lethargy, polyuria, shorten QT complex, heart arrhythmias *potentiates the effects of Digoxin (causes bradycardia HR <60)
Treating hypercalcemia IV hydration, Calcitonin (combats calcium), non-thiazide diuretics
Hypomagnesium symptoms Changes in personality, nystagmus (eyes twitch), Babinski's sign, ^BP/HR, arrhythmia
Hypermagnesium symptoms Confusion, lethargy, v BP, coma, cardiac arrest, arrhythmia
Hypophosphate symptoms Tremors, bone pain, joint stiffness, bleeding disorders, seizures
Hyperphosphate symptoms Weakness, N/V, dysphagia, tetany, v BP
Trousseau's sign BP cuff on arm and arm will start to contract
Normal blood pH 7.35 - 7.45
Normal paCO2 35-45 (regulated by lungs) Respiratory system
Normal paHCO3 22-26 (regulated by kidneys) Metabolic system
Metabolic Acidosis symptoms Weakness, fatigue, LOC changes, bradycardia, arrhythmia, hyperkalemia, stupor, coma, *Kussmaul's respiration (rapid deep breathing to get rid of excess CO2)
Metabolic Alkalosis symptoms Confusion, *hyperreflexia, tetany, dysarrhythmias, seizures, reps failure, hypokalemia
Respiratory Acidosis symptoms Acute: Flushed skin, blurry vision, v LOC Chronic: weakness, impaired memory, sleep disturbances, dull headache
Respiratory Alkalosis symptoms Dizziness, palpations, dyspnea, chest tightness, anxiety, panic, tremors, tetany, seizures, loss of consciousness
Causes of Metabolic acidosis DKA, renal failure, diarrhea (excess gastric acid)
Causes of Metabolic alkalosis Excessive vomiting, GI suctioning, or too much bicarb (loss of gastric acid)
Causes of Respiratory acidosis COPD, near drowning, suffocation, respiratory failure, lung diseases (retaining too much CO2)
Causes of respiratory alkalosis Hyperventilation, anxiety (breathing off too much CO2)
Tidal Volume The amount of air moved in and out of the lungs in one normal breath
Inspiratory volume The amount of air that can forcibly be inhaled over tidal volume
Expiratory volume The amount of air that can be exhaled forcibly over tidal volume
Residual volume The value of air left in the lungs after a forced exhale
Vital capacity The sum of TD, IV, and EV (about 4500mL)
WBC count that signals infection is present >11,000
Normal pulse ox and COPD pulse ox >90% and >88%
Pulmonary angiogram Checks circulation pattern through lungs
Pulmonary V/Q scan Injected dye/inhaled gasses to check ventilation and perfusion
Thoracentesis Drains fluid from the pleural space to increase comfort
Pleuritis Inflammation of the plural sac secondary to a lung infection or trauma
Plural effusion Collection of fluid in the plural space. Dx with x ray, lungs sound diminished; tx underlying cause
Pneumothorax Collection of air in the plural space., can be spontaneous (primary or secondary cause), Traumatic (open/closed/latrogenic), or Tension. Dx with chest x ray. Tx with chest tube
Symptoms of spontaneous/traumatic pneumothorax Chest pain, dyspnea, SOB, tachypnea, tachycardia, diminished/absent lung sounds
Symptoms of tension pneumothorax Life threatening: hypotension, shock, distended jugular veins, severe dyspnea, tachypnea, tachycardia, absent breath sounds, tracheal deviation
Hemothorax Collection of blood in the plural space
Flail chest 2 or more consecutive rib breaks result in free floating portions of rib. Tx with pain control
Inhalation injuries Smoke (fire/chemical burns results in airway damage) and Near-drowning (asphyxiation/aspiration injuries)
Pulmonary Embolism prevention teds, SCDs, heparin, Lovenox, mobility
Manifestations of pulmonary embolism Sudden onset: dyspnea, SOB, chest pain, anxiety, cough, tachycardia, crackle, low-grade fever
Acute respiratory failure Lungs are unable to meet demands of body (obstruction, COPD, PE, trauma, et.)
Symptoms of hypercapnia dyspnea, respiratory depression, swelling of optic disc, tachycardia, DROWSINESS, respiratory acidosis
Symptoms of hypoxemia dyspnea, tachypnea, RESTLESSNESS, tachycardia, metabolic acidosis
Created by: jperrault9941