NRSG 3420 Mod 1 Blood and Immune Disorders - Quizlet PDF

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mean arterial blood pressure/Single best indication of tissue perfusion is MAP >65 mmHg/what reading is used to assure adequate tissue perfusion of tissue organs  (SBP + 2 DBP)/3 o Hemoglobin concentration o Oxygen saturation of hemoglobin o Oxygen concentration at the lung  Blood and Components o 4-6 liters in average adult o Plasma: thin colorless liquid that contains proteins (albumin, globulin, fibrinogen, clotting factors), electrolytes, nutrients, and waste products  55% of volume  the difference b/w plasma and serum is that serum lacks clotting factors o Cellular components: 45% of volume  RBC, WBC, platelets  Hematopoiesis o Bone marrow is primary site of blood cell formation o Primitive stem cells – ability to self-replicate  Myeloid: RBCs, WBCs, and platelets  Lymphoid: T and B lymphocytes o Erythropoietin = hematologic growth factor released from kidney -> stimulates RBC o Aging  Amount of bone marrow and number of stem cells decreases  More vulnerable to oxygen transport, fighting infection, and clotting o Hematopoietic growth factors regulate proliferation, differentiation, and viability of cells  Cell Amounts o RBCs – erythrocytes  Many: polycythemia  Few: anemia o WBCs – leukocytes  Many: leukocytosis, lymphocytosis  Few: leukopenia, neutropenia o Platelets – thrombocytes  Many: thrombocythemia  Few: thrombocytopenia  RErythrocytes (Red Blood Cells)  RBC Production o Myeloid stem cells -> erythroblast under influence of erythropoietin  Erythropoietin – produced in kidney, carried to bone marrow o Erythroblast gradually loses nucleus and when mature -> released into circulation ( o Process of maturation takes 5 days o hypoxia = primary stimulus to increase RBCs  Erythrocytes

Thin membrane so O2 can easily diffuse across it Biconcave shape Mature RBCs consist primarily of Hgb Mature RBCs have no nucleus and few metabolic enzymes Normal red cell count: 4.2-6.2 million/mm3  Men have more than women o Reticulocytes = immature RBCs  Increased demand (ex. hemorrhage), immature cells are released into circulation  Monitor reticulocyte count Nutritional Factors affect RBC production o Iron = essential component of hemoglobin  Found in meat, lentils, beans, enriched foods  Iron deficiency -> bone marrow depressed  RBCs = small and low and Hgb o Microcytic and microchromic  Excessive iron can cause tissue damage (esp in liver, heart, pancreas, and testes) -> becomes a problem when ppl require long term infusion therapy o Vitamin B12 and folic acid = essential for DNA synthesis  Vitamin B12 found only in foods of animal origin (vegetarians at risk)  Folic acid found in leafy green veggies, fruits, legumes, and beans RBC Function o Hemoglobin carries oxygen to tissues and CO2 to lung  4 globins: 2 alpha and 2 beta  single RBC can contain as many as 120 Hgb  15 g Hgb/100 mL of blood o Life span of a RBC in circulation is approx. 120 days RBC Destruction o Aging RBCs lose elasticity and may become trapped in small blood vessels and spleen o Removed from circulation by reticuloendothelial cells in liver and spleen  Hgb is recycled -> breaks down to bilirubin and secreted in bile  Iron is recycled to form new Hgb o o o o o

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Leukocytes (White Blood Cells)  Leukocytes o Leukocytes 4,000 – 11,000 cells/mm3  Granulocytes  Neutrophils 55% o Polymorphonuclear or segmented neutrophils o Bands – mature, segs – immature o Ingest and destroy bacteria, but do not survive process  Eosinophils 1-4% o See increase in allergic disorders or parasitic infections  Basophils same composition as plasma w/o clotting factors or fibrinogen o Plasma Proteins: albumin and globulin  Transport globulins carry other things through circulation  Ex. Transferrin carries iron  Immunoglobulin  Gamma globulin = group of immunoglobulins (antibodies)

o Clotting factors are inactivated in plasma until they are activated by clotting cascade Assessment of Hematologic Disorders  Reticular Endothelial System o Removes old or damaged cells from circulation o Consists of BM, thymus, liver, spleen, lymph nodes, phagocytic system o Stimulates inflammatory response o Recognize foreign cells and trigger the immune response  CBC (Red Blood Cells) o Obtained by venipuncture, broad hematologic screening test o Not uncommon for abnormalities to be detected in pts who are asymptomatic o Normal Values  RBCs: 4.2 – 6.2 mill/mm3  Hgb: 14-16 male, 13-14 female  HCT: 36-46%  MCV: 84 – 96 mcg3  MCHC: 31-35%  RDW: Hgb: Hct = 1:3 o Hgb is major determinant of RBC size  If Hgb is low, RBCs are often small and pale  MCV 60% associated with spontaneous clotting CBC (WBC) o Normal: 4,500 to 11,000/cu3  Neutrophils: 45-73%  Eosinophils: 0-4%  Basophils: 0-1%  Lymphocytes: 20-40%  Monocytes: 2-8% o Neutrophils – elevated in infection o Eosinophils – elevated in allergic or parasitic responses o Basophils – elevated in allergens o Lymphocytes – elevated in viral infection o Monocytes – elevated in Epstein Barr infection Calculating the ANC o Normal: 7,500 cells/cc o From the CBC: add percentage of segs and bands, multiply combined percentage by total WBC Nursing Alert! o Increased risk for infection o Hand washing critical o Reverse isolation procedures have not been shown to be effective CBC (Platelets) o Normal: 150,000-450,000/mm3 o Thrombocytopenia  In absence of fever or infection, 5,000/mm3 may be sufficient prevent spontaneous bleeding  For invasive procedures want at least 50,000/mm3 o Thrombocythemia  Infrequent  Greater than 600,000 present for at least 2 months BM Aspiration and Biopsy o Aspiration (removes just marrow)  Aseptic skin cleansing – usually taken from iliac crest  Local anesthetic – pressure sensation  Pain as needle passes through periosteum and bone marrow aspiration o Biopsy (removes bone and bone marrow)  Small skin puncture  Pressure but not pain  After  Pts may feel aching at the site for 1-2 days  Acetaminophen (NOT aspirin) can be used  Do not submerge in water for 24-48 hrs o Post Care 

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Local pressure applied for several minutes then sterile dressing

Care of Patients with Anemia  Anemia o Decrease in number of RBCs, Hgb, or Hct o not a diagnosis, it is a sign of an underlying problem o classified by pathophysiologic basis  Decreased or defective production of RBCs (hypoproliferative includes megaloblastic)  increased destruction of RBCs (hemolytic)  blood loss o most common hematological disorder in older patients  40% of older patients in hospitals have anemia  Signs and Symptoms o Influenced by severity, rapidity of onset, duration, metabolic requirements and comorbidities  Underlying cardio-pulmonary level may experience fatigue at a higher hgb level than someone without underlying conditions o Decreased oxygen carrying capacity  Dyspnea, palpitations, fatigue, dizziness o Decreased tissue perfusion  Claudication, angina, weakness, pallor o Symptoms rarely occur until hgb shape changes becoming sickled  Less able to squeeze through smaller blood vessels, deliver less O2 to tissues  May be seen on peripheral blood smear  CBC: low Hgb, low Hct, elevated WBC  Symptoms  Cardinal sign: recurrent painful crises  Anemia: fatigue tachycardia, murmur, jaundice  Increased susceptibility to infection (esp. pneumonia and UTIs)  Increased susceptibility to thrombosis (TIAs, infarction, difficulty thinking)  Sickle Cell Crisis  Risk factors: infection, dehydration, cold, hypoxia  Symptoms: severe pain (last hours or days) o Most likely in long bones or chest  Management o Pain control o O2 therapy o Hydration 

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o Transfuction o Hydroxyurea for patients with >3 crises a year to reduce crises Nursing Dx o Acute pain o Risk for infection o Powerlessness and illness-related helplessness o Knowledge deficit Nursing Interventions o Pain management o Prevent and manage infection o Promote effective coping o Promote understanding of disease  Trajectory of chronic disease o Minimize and manage complications

Bleeding and Clotting Disorders  Balance between Hemostasis and Fibrinolysis o Hemostasis –minimizing blood loss  Platelet function – activated when exposed to interstitial collagen from injured blood vessel  Endothelial function  NO and PGI2  Thrombin inhibitors  Clotting cascade o Fibrinolysis  Plasminogen Plasmin system  Plasminogen  Plasmin – dissolves fibrin, clot breaks down  Activated by t-PA, clotting factors and kallikrein  Fibrin degradation products (FDP)  D-dimer  Thrombocytopenia o Decreased platelet production o Increased platelet destruction o Increased plateles consumption  Nursing Process o Assessment  When platelet count drops below 20,000  petechiae may be seen along oral mucosa or trunk and legs  oozing gums or bleeding from venipuncture sites  epistaxis – nose bleeds o high fowlers, ice pack to back of neck, pressure to bridge of nose  when the platelet count drops below 5,000  fatal intracranial or GI hemorrhages o Nursing Diagnosis

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 Risk for bleeding o Nursing Intervention: bleeding precautions  Avoid aspirin and aspirin containing products  Avoid IM injections  Use small bore needle for venipuncture  Toothettes or soft bristle toothbrush for oral care  Stool softeners, avoid vigorous coughing/blowing of nose  Safety – falls prevention Coagulation Disorders o Inherited disorders: hemophilia and Von Willebrand’s disease o Drugs effects:  Aspirin – effects platelets for 1 week  Warfarin – vitamin K antagonist, dosing determined by INR (2-3)  Heparin o Liver disease – may intensify drug effects o Disseminated intravascular coagulopathy (DIC)  A sign not a disease  SEVERE life-threatening syndrome, mortality rate: 80%  Massive number of small clots form in the microcirculation and “use up” clotting factors -> bleeding  Search for underlying cause: sepsis, trauma, cancer, shock, toxins, placenta abruptio, allergic reaction  Labs  Low platelet count, low fibrinogen count, prolonged PT, PTT and thrombin time prolonged  Initial sign = progressive decrease in platelet count, followed by thrombosis, then bleeding  Medical Management of DIC  Treat underlying cause  Improve oxygenation and perfusion  Replace coagulation factors  Other approaches: interrupt thrombosis w/ heparin infusion (may increase risk of hemorrhage)  Nursing Considerations  At risk: sepsis and acute leukemia  Monitor for thrombosis and bleeding o Skin: temp, cyanosis o Circ: pulses o Resp: hypoxia, dyspnea, chest pain o Renal: urine output o GI: heartburn, GI bleeding o Neuro: change in mental status, pupil reaction, pain o Heparin induced thrombocytopenia syndrome (HITS)  Allergic reaction to heparin  Antibody against heparin-platelet-factor 4 complex  >50% drop in platelet count after exposure to heparin

Continued exposure -> thrombotic complications – arterial and venous Action: stop heparin immediately  Blood specimen sent to lab for antibodies  Direct thrombin inhibitor used as alternative to heparin Thrombotic Disorders o Inherited:  Factor V Leiden mutation  Protein C deficiency  Protein S deficiency  Antithrombin deficiency  Increased factor VIII activity o Acquired  Immobilization  Obesity  Pregnancy  Oral contraceptives  Heart failure  Malignancies  Polycythemia Vera (PV)  Increased production of RBCs, WBCs, and platelets (mostly RBCs) o Hct >50% in women or >55% in men  More common in men, rare in people under 40 years old  Outpatient management  S/S o Increased blood viscosity and total blood volume o Generalized pruritus (histamine release from basophils)  May be made more intense by warm shower or bath o Headache, dizziness, fatigue, paresthesias, HTN o Angina, claudication, thrombophlebitis  Avoid dehydration in patients with PV  Management o Phlebotomy – may be done weekly until Hct 1 C rise in body temp, chills, shaking  Intervention  Stop transfusion  Follow transfusion reaction protocol  If known to have this reaction: pre-medicate with acetaminophen or benedryl before transfusion

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o Allergic Reactions  mild (hives, urticaria)  stop transfusion  administer anti-histamine  resume transfusion if symptoms abate with anti-histamine  severe (anaphylactic)  stop transfusion  administer anti-histamine, steroids, and vasopressors as needed  pre-medicate with anti-histamine and steroids o Volume Overload  Risk factors: advanced age, low cardiac contractility  Prevention  Diuretic before or between units  Manifestations  Cough, dyspnea, crackles, tachycardia, HTN  Action  Infuse slowly, elevate HOB, lower feet, O2, diuretics, morphine (meds as prescribed o Other Risks  Electrolyte Imbalance  Sodium citrate is the preservative in blood banks o Citrate bind calcium -> reduction in serum calcium, coagulopathy, tetany, and cardiac arrhythmia  Massive transfusion  Monitor ionized calcium and mag and replace as needed  Hyperkalemia – stored blood liberates potassium o Monitor potassium o Check expiration date on blood products  Iron overload with multiple or frequent transfusions  Early symptoms: vomiting, diarrhea, hypotension  Deferoxamin turns urine red as iron is taken out of the system  Iron chelation therapy To Note: o Colloids for volume expansion  Hetastarch,, albumin  Osmotically active solution to keep fluid within vascular space

o Blood conservation and salvage  Minimize phlebotomy losses  Surgical drain salvage o Pharmacological therapy  Erythropoietin – anemia  Granulocyte colony-stimulating factor – neutropenia  Aminocaproic acid (Amicar) – decreased fibrinogen  Desmopressin (DDAVP) – uremic bleeding  NovoSeven RT (Factor VII)

Immunologic Conditions  Immunity = body’s protective response against foreign substance o Antigen = substance that illicits an immune response, usually a protein o Natural immunity  Present at birth  Non-specific defense against invaders  Physical and chemical barriers  Inflammatory response  Immune regulation o Acquired immunity  Humoral antibody response – B lymphocytes  Cellular immune reponse – T lymphocytes (attack foreign invaders directly) o Inflammatory Response  Localized protective response of tissues to injury or invasion  Intended to neutralize, control, or eliminate offending agent and prepare site for repair  Non-specific, immediate response  Granulocytes release chem substances (histamines, bradykinin, and prostaglandins) and engulf invaders  Non-granulocytes engulf and destroy invaders  Vascular response  Vasodilation, increased vascular permeability, and WBC migration  Neutrophils = nature’s first responders  Plasma protein systems  Complement system o Enhanced phagocytosis, increased vascular permeability and cellular lysis  Prostaglandins and leukotrienes o Drugs that inhibit prostaglandins can reduce inflammation  Manifestations of Inflammation  Cardinal Signs o Pallor – initial vasoconstriction o Rubor (redness) - vasodilation o Calor (warmth) – increased metabolism at site of inflammation o Dolor (pain) - stimulation of nerve endings

o Loss of function – swelling and pain Systemic effects o Fever – triggered by release of cytokines -> activate defense mechanisms  Benefits: killing microorganisms, increased phagocytosis, increased T cell proliferation o Leukocytosis o Plasma protein synthesis o Inflammation – immediate, short-lived, non-specific o Immune response – delayed, long-lived, specific Immune Response o Humoral immunity  Characterized by production of antibodies by B lymphocytes in response to a specific antigen  Involved in bacterial phagocytosis and lysis, anaphylaxis, allergic rhinitis, and asthma  5 classes of immunoglobulins  Antibody-antigen reaction  B lymphocytes o Cell-mediated immunity  T lymphocytes  Attack invaders directly 

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Factors that Affect Immune Function o Advancing age – B and T cell function reduced o More autoimmune disease in women – maybe related to sex hormone o Nutrition  Vitamin D deficiency associated with increased risk of infection, cancer, autoimmune disease  Micronutrients – zinc and selenium o Co-morbid conditions  Diabetes o Exposures o Genetic factors o Lifestyle o Medications – alcohol and some meds can suppress immune function o Stress Disorders of Immune Function o Hypersensitivity  Allergy, anaphylaxis, autoimmunity o Deficiency states  Primary deficiency, acquired deficiency Anaphylaxis o Specific antigen - IgE antibody reaction o Systemic release of mediators (histamine, prostaglandins, and inflammatory cytokines) from mast cells  Edema and pruritis  Bronchospasm, airway obstruction, vascular collapse o Common causes of anaphylaxis  Foods, medications, bee stings, latex o Management  Epinephrine (Epi-Pen and/or infusion)  Observation: re-bound 4-10 hrs later o Clinical Management  Prevention  Avoid exposure  Carry and administer epinephrine  Screening for allergies before med is first administered  Medic alert bracelet  Venom immunotherapy  Activate emergency medical system (911) after admin epi Allergic Rhinitis o Induced by airborne pollen or molds  Local release of histamine in the nasal mucosa o Incidence increases with age o If untreated, may lead to chronic otitis, allergic asthma, or loss of sense of smell o Management  Symptom relief

Antihistamines – receptor blockers, best given at onset of symptoms o Not indicated for anaphylaxis  Decongestants (Adrenergic agents) – vasoconstriction mucosal vessels, reducing mucosal edema  OTC nasal sprays – pt may experience rebound effect after as little as 2-3 days of reg usage  Mast cell stabilizers – reduce release of histamine, takes up to a week to work o Ex. Intranasal chromalin  Corticosteroid sprays – reduce tissue inflammation, takes several days up to 2 weeks to work  Avoidance therapy  Immunotherapy Immunotherapy o Form of desensitization to specific allergen  Slow (3-5 years) increasing doses of allergen given to increase blocking of immunoglobulins and reduce mast cell sensitivity  Come in weekly to q2 weeks o Allergen must first be identified o Shown to be most effective against ragweed pollen o Injection may induce systemic reaction and must be administered in a setting where epinephrine and emergency measures are immediately available  Early s/s: pruritis, urticarial, sneezing, laryngeal edema, hypotension Nursing Care for Allergies o Identify and document known allergies o Encourage medic alert band o Assess allergic hx before first admin of medication; monitor response to new meds o Identify early manifestations of allergic reactions o Patient and family education re: avoidance measures Autoimmune Condition o Inappropriate reaction to self proteins, immune system no longer differentiates self from non self o Tend to cluster, 10x more common in women, 3x more common in AA women than white women o Common autoimmune disorders: multiple sclerosis, Guillan Barre, autoimmune hemolytic anemia, thyroiditis, myasthenia gravis o Systemic lupus erythematosus is a chronic multisystem autoimmune disorder  Pathophysiology: breakdown of tolerance  Both B and T cells are implicated  High prevalence among families  Overall prevalence 1:2,500  Clinical Manifestations  Typically affects skin, joints, serous membranes  Renal, hematologic, and neurological  Marked variation in severity, mild to rapidly progressive  General - Fever, fatigue, weight loss 

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Musculoskeletal – myalgias, joint swelling, pain with movement, morning stiffness o Lupus related arthritis is non-erosive, but may cause deformities  Integumentary – butterfly rash (cheeks, nose, forehead), oral ulcers, vascular lesions on sun-exposed areas o Advised to stay out of sun or use sunscreen  Hematologic – anemia, leukopenia, thrombocytopenia  Cardiopulmonary – pericarditis, early atherosclerosis, pleuritis, dysrhythmias from cardiac fibrosis  Renal – lupus nephritis occurs in 50% pts within 1 year of diagnosis  CNS – subtle changes in co...