ANCC AGACNP Barkley Review Questions and Answers

ANCC AGACNP Barkley Review Questions and Answers Hemoglobin (Hgb) Main component of RBC's and the essential protein that combines with and transports O2 to the body. Males: 14-18 g/100 mL Females: 12-16 g/100 mL Hematocrit (Hct) Measures the percentage of a given volume of whole blood that is occupied by erythrocytes: the amount of plasma to total RBC mass (RBC concentration). Females: 37-47% Males: 40-54% Total Iron Binding Capacity (TIBC) Increased levels indicate iron deficiency (the greater their TIBC, the greater their need for iron).; Decreased levels may indicate anemia, hemorrhage, hemolysis. Normal: 250-450 mcg/dL Serum iron Normal: 50-150 ug/dL Mean Corpuscular Volume (MCV) Expression of the average volume and size of individual erythrocytes. Normal: 80-100 um3 Microcytic = 80, Normocytic = 80-100, and Macrocytic = 100. Mean Corpuscular Hemoglobin (MCH) Expression of the average amount and weight of Hgb contained in a single erythrocyte. Normal: 26-34 pg Mean Corpuscular Hemoglobin Concentration (MCHC) Expression of the average Hgb concentration or proportion of each RBC occupied by Hgb as a percentage; more accurate measure than MCH. Normal: 32-36% Hypochromic 32%, normochromic 32-36%, hyperchromic 36% Differential for low mean corpuscular volume (MCV) Iron deficiency anemia and thalassemia. Differential for high mean corpuscular volume (MCV) B12 or folate deficiency (Megaloblastic anemia), alcoholism, liver failure, and drug effects. Differential for normal mean corpuscular volume (MCV) Anemia of chronic disease, sickle cell, renal failure, blood loss, and hemolysis. Iron deficiency anemia is what type if anemia? Microcytic, Hypochromic. Iron deficiency anemia A microcytic-hypochromic type of anemia characterized by iron deficiency that affects the production of hemoglobin and is characterized by small red blood cells containing low amounts of hemoglobin. Signs and symptoms of iron deficiency anemia Usually few symptoms if Hct is greater than 30. As Hct decreases, symptoms present: pica, dyspnea and mild fatigue with exercise, HA, palpitations, weakness, tachycardia, postural hypotension, and pallor. Laboratory findings in iron deficiency anemia Low Hgb, low Hct, low MCV, low MCHC, low RBC, low serum iron, low serum ferritin (iron storage), high TIBC , *high RDW (red cell distribution width. *Indicates there is a large difference in size from the largest to smallest RBC. How is iron deficiency anemia treated Ferrous sulfate orally 300-325 mg 1-3 hour after meals. Do not take iron supplements with antacids, it can interfere with absorption. Take with vitamin C containing juices. Increase iron intake: Raisins, green leafy vegetables, red meats, citrus products, and iron-fortified bread and cereals. What type of anemia is thalassemia Microcytic, hypochromic. Thalassemia Genetic inherited disorders resulting in abnormal Hgb production and microcytic, hypochromic anemia. Mostly found in Mediterranean, African American, Middle Eastern, Indian, and Asian populations. Etiology of thalassemia There is a decreased production of adult hemoglobin (Hb A); The global part of Hb A has 4 protein sections called polypeptide chains - (1) two of these chains are called alpha chains and are identical, (2) the other two are identical but different from the alpha chains, called beta chains. What is the most common type of thalassemia Beta thalassemia What is the cause of beta thalassemia There is a reduction or absent production of beta globin chains. Thalassemia Minor Heterozygous form of beta thalassemia; they only have one copy of the beta thalassemia gene with a normal beta chain gene. Thalassemia Major (Cooley's Anemia) Homozygous form of beta thalassemia; they have two genes for beta thalassemia and no normal beta chain gene. Signs and symptoms of Thalassemia Major In early life: failure to thrive, feeding difficulties, bouts of fever, diarrhea, hepatosplenomegaly and jaundice, maxillary enlargement. Laboratory findings in Thalassemia Major Decreased Hgb, Low MCV, low MCHC, normal TIBC, normal ferritin, decreased alpha or beta Hgb chains. Treatment for Thalassemia Major No treatment for mild or moderate forms; RBC transfusion/splenectomy for more severe forms; Do not give iron, because of the possibility of iron overload. Folic acid deficiency A microcytic, normochromic anemia (Megaloblastic anemia) resulting from folic acid deficiency. What group of people often have folic acid deficiency Alcoholics; Can be treated with Folic Acid, Vitamin B1 (Thiamin), and/or a banana bag. Signs and symptoms of folic acid deficiency Fatigue, dyspnea on exertion, pallor, headache, tachycardia, anorexia, and glossitis. * No neurological changes are noted, which is how B12 deficiency can be differentiated from folic acid deficiency. Glossitis Inflammation of the tongue. Laboratory findings in folic acid deficiency Hct and RBC decreased, MCV elevated (macrocytic), MCHC normal (normochromic), serum folate decreased, red blood cell folate less than 100 ng/mL. * Normal red blood cell folate 140-628 ng/mL Treatment for folic acid deficiency Folate 1 mg orally every day; foods high in folic acid: bananas, peanut butter, fish, green leafy vegetables, iron-fortified breads and cereals. Sickle Cell Anemia A genetic disorder that causes abnormal hemoglobin, resulting in some red blood cells assuming an abnormal sickle shape. Sickle Cell Anemia affects the African American population. Cellular hypoxia causes acidosis and tissue ischemia. Pain occurs as a result of the ischemia and blood hyperviscosity. Sickle cell anemia crisis symptoms Sudden severe pain in extremities, back, chest, and abdomen; aching joint pain; weakness; dyspnea. What factors can cause sickling of the cells in sickle cell anemia Hypoxia, infections, high altitudes, dehydration, physical or emotional stress, surgery, blood loss, and acidosis. Laboratory findings in sickle cell anemia Decreased hemoglobin (carries oxygen), and peripheral blood smear shows sickle-shaped RBCs. Treatment for sickle cell anemia Fluids for dehydration, pain medication (Dilaudid), supplemental oxygen for hypoxemia. Medication used for sickle cell anemia Hydroxyurea Von Williebrand Disease A genetic disorder that results in the reduced ability to create blood clots; caused by deficiency in von Williebrand factor and clotting factor VIII (8). Signs and symptoms of Von Williebrand Disease Prolonged, frequent, or severe episode of bleeding; easily bruised. Treatment for Von Williebrand Disease Desmopressin (DDAVP), recombinant von Williebrand factor (VWF)/factor VIII concentrate (exogenous form). *DDAVP works by making the body release more VWF into the blood. It also helps increase the level of factor VIII in the blood. Leukemias Neoplasm arising from hematopoietic cells in the bone marrow. More frequently noted in males. Acute Myelogenous Leukemia (AML) Constitutes 80% of acute leukemia in adults, remission rates from 50 to 85%, long-term survival is 40%. Acute Lymphocytic Leukemia (ALL) More difficult to cure in adults than children (90% remission rate in children). *Hallmark of disease: Pancytopenia with circulation blasts. Chronic Lymphocytic Leukemia (CLL) Most common leukemia in adults; median survival is 10 years occurs in both middle and old age. *Hallmark of disease: Lymphocytosis. Chronic Myelogenous Leukemia (CML) Occurs most often in persons aged 40 or older; Survival: approximately 65% of those diagnosed are still alive at 5 years. *Hallmark of disease: Philadelphia chromosome seen in leukemic cells Signs and symptoms of leukemia May be asymptomatic, fatigue, weakness, anorexia, generalized lymphadenopathy, weight loss. Laboratory findings in leukemia CBC with subnormal RBS's and neutrophils; elevated erythrocyte sedimentation rate (ESR); peripheral blood smell usually distinguishes chronic and acute leukemia, but a bone marrow biopsy aspiration is required to confirm the diagnosis. What is used to confirm a leukemia diagnosis Bone marrow aspiration Treatment for leukemia Chemotherapy, bone marrow transplantation, and control of symptoms. *Initiate Allopurinol to reduce tumor lysis syndrome in high risk patients. Tumor lysis syndrome Chemotherapy can cause massive destruction of cells leading the creation of uric acid which can be toxic to the kidneys leading to Acute Tubular Necrosis. You can try to prevent this with hydration and Allopurinol. Signs and symptoms of Tumor lysis syndrome Uricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Lymphomas Lymphocytic malignancy. Staging of lymphoma Stage 1: Disease localized to single lymph node or group Stage 2: More than one lymph node group involved; confined to one side of the diaphragm Stage 3: Lymph nodes or spleen involved; occurs on both sides of the diaphragm Stage 4: Liver or bone marrow involvement How is lymphoma stage diagnosed Biopsy of the enlarged lymph nodes Non-Hodgkin's Lymphoma Most common neoplasm between the ages of 20-40. May present with lymphadenopathy; less predictable pattern of spread than Hodgkin's. *Increased risk at 57 years old Hodgkin's lymphoma More common in males, average age is 32. Usually presents with cervical adenopathy and spreads in a predictable fashion along lymph node groups. *Characteristic Reed-Sternberg cells differentiation from Non-Hodgkin's Lymphoma. Laboratory findings in Lymphoma CT, Xray, Ultrasonography, MRI used to locate and stage the disease. What confirms the diagnosis of lymphoma Biopsy and histopathologic examination Idiopathic Thrombocytopenic Purpura (ITP) Thrombocytopenia resulting from autoimmune destruction of platelets with or without suppression of thrombopoiesis. Women outnumber men by 3:1. Occasionally patients with ITP require hospitalization due to bleeding. Normal platelet count: 150,000 - 450,000 Diagnostics used for Idiopathic Thrombocytopenic Purpura (ITP) Bone marrow analysis, low platelet count with other causes of thrombocytopenia ruled out; there may be aa history of early bruising or bleeding. Treatment for Idiopathic Thrombocytopenic Purpura (ITP) Treatment may not be necessary until platelets reach 20,000; High dose corticosteroids to help elevate the platelet count within 2-3 days; IV gamma globulin, which typically responds within 2-3 days; platelet transfusion may be beneficial. *Gamma globulin is preferred to steroids in HIV-related ITP. Idiopathic Thrombocytopenic Purpura (ITP) patient precautions Avoid constipation (increase fiber, laxatives, etc. ); no flossing, no shaving, hold pressure for 5 minutes or more for cuts, line insertions, etc. Heparin-induced thrombocytopenia (HIT) Results from antibody to heparin- p54 complex, this causes thromocytopenia in 1-5% of patients on heparin therapy. Lepirudin (Refludan) or Argatroban (Acova) can be used to manage HIT. How can Idiopathic Thrombocytopenic Purpura (ITP) be differentiated from Systemic Lupus Erythema (SLE) A bone marrow analysis is necessary to differentiate due to both causing thrombocytopenia. Disseminated Intravascular Coagulation (DIC) An acquired coagulation disorder which results from the intravascular activation of both the coagulation and fibrinolytic systems (thrombin and plasmin are activated), causing simultaneous thrombosis and hemorrhage; mortality rate is 50-85%. Conditions that can cause Disseminated Intravascular Coagulation (DIC) Malignant neoplasms, infections/sepsis, liver disease, massive trauma, extensive burns, shock, obstetrical complications, acute leukemia. Pathophysiology of Disseminated Intravascular Coagulation (DIC) Thrombin causes conversion of fibrinogen to fibrin, producing fibrin clots in the microcirculation. Thus reducing coagulation factors, i.e., fibrinogen, prothrombin, platelets, factors V and VII. Circulating plasmin activates the fibrinolytic systems which lyses fibrin clots into fibrin degradation products (FDPs). Hemorrhage results from the anticoagulant activity of FDPs and the depletion of coagulation factors. Signs and symptoms of Disseminated Intravascular Coagulation (DIC) Acute DIC findings: ecchymosis, oozing from venipuncture sites and petechiae to mucous membranes. Laboratory findings in Disseminated Intravascular Coagulation (DIC) Thrombocytopenia (platelets 150,000), hypofirinogenemia (fibrinogen 170 mg/dL), decreased RBCs, increased fibrin degradation production (FDPs) ( 45 mcg/ml or present at 1: 100 dilution), prolonged prothrombin time (PT) ( 19 seconds), prolonged partial prothrombin time (PTT) ( 42 seconds), and D-dimer (+ at 1:8 dilution). * With increased FDPs, there is a predictive accuracy of 96% for diagnosis of DIC Treatment for Disseminated Intravascular Coagulation (DIC) Treat the underlying condition and control bleeding. Platelet transfusion for thrombocytopenia, fresh frozen plasma (FFP) to replace clotting actors, and cryoprecipitate to maintain fibrinogen. Pain Acute pain: duration is usually short and less than 6 months. Chronic pain: continual or episodic pain that usually lasts more than 6 months. Cutaneous pain Pain localized on the skin or surface of the body. Visceral pain Poorly localized such as with internal organs. Somatic pain Non localized; originates in muscle, bone, nerves, blood vessels and supporting tissue. Neuropathic pain Frequently cause by a tumor; involves nerve pathway injury or compression. World Health Organization (WHO) ladder of pain management A 3-step system progressive ladder starting with Aspirin, Acetaminophen, or NSAID. Continues to build through the 3-steps with heavier narcotics added, while maintaining the initial choice os Aspirin, Acetaminophen, or NSAID. Step 1: ASA Acetaminophen NSAID +- Adjuvants Step 2: ASA or Acetaminophen Codeine Hydrocodone Oxycodone Dihydrocodeine Tramadol (not available with ASA or acetaminophen) +- Adjuvants Step 3: Morphine Hydromorphone Methadone Levorphanol Fentanyl Oxycodone +- Adjuvants +- Non-opioid analgesics Treatment used for break-through cancer pain Fentanyl patches for sustained release. Treatment used for bone pain Bisphosphonates (inhibitors of bone resorption, acting by inducing osteoclast apoptosis and thereby preventing the development of cancer-induced bone lesions). Pressure Ulcer Any lesion caused by unrelieved external pressure resulting in occlusion of blood flow. Stage 1 Pressure Injury Intact skin with erythema that does not blanch; color changes do not include purple or maroon discoloration. Stage 2 Pressure Injury Partial-thickness loss of skin with exposed dermis; wound bed is viable, pink or red, moist, and may also present as an intact or ruptures serum-filled blister' adipose and deeper tissues are not visible. Stage 3 Pressure Injury Full-thickness skin loss; adipose is visible in the ulcer and granulation tissue and edible (rolled wound edges) are often present; slough and/or eschar may be visible. *If slough or eschar obscures the extent of the tissue loss then it is unstageable Stage 4 Pressure Injury Full-thickness skin and tissue loss; full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location. *If slough or eschar obscures the extent of the tissue loss then it is unstageable Unstageable Pressure Injury: Obscured full-thickness skin and tissue loss Full-thickness skin and tissue loss; the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar; if slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed; stable eschar (i.e., dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed. Deep Tissue Pressure Injury (DTPI): Persistent non-blanchable deep red, maroon or purple discoloration Intact or non-intact skin with localized areas of persistent non-blanchable deep red, maroon or purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister; if necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible = full thickness pressure injury (which can be classified as a stage 3, stage 4, or unstageable pressure injury); do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions. Considerations in pressure ulcers Hypoalbuminemia: normal levels is 3.5 - 5 (reliable factor for pressure ulcer development); Wound care consult; dress with hydrocolloid dressing if weeping. What are concerning diagnosis that can be caused by pressure ulcers Osteomyelitis and sepsis Fever Used to describe a temperature above normal (37.0 °C or 98.6 °F. Commonly used to determine the presence of an infection. *37.7 °C or 99.8 °F