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49 Cards in this Set
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Components and functions of hematology systems. Blood, speed, bone marrow, lymphatic system, EPO, thrombopoietin |
• Bone marrow (primarily red bone marrow) o Blood cell production (erythrocytes (RBC), leukocytes (WBC: neutrophils, eosinophils, basophils, lymphocytes, monocytes), thrombocytes/platelets through hematopoietic stem cells by negative feedback, ex less RBC = increased production) • Spleen o Destruction of RBCs (splenomegaly -> increased RBC destruction), reservoir for immune cells, filters blood of defective RBCs o Splenomegaly causes -> sign of hepatic/hematological problem [Liver disease (e.g., cirrhosis), hematologic malignancy, infection (e.g., AIDS, endocarditis), congestion or inflammation (e.g., congestive failure), primary splenic disease (e.g. splenic vein thrombosis)]
• Blood o RBC, WBC, platelets, plasma (largest component) [45% blood cells (RBC, WBC, Plts), 55% plasma] o Protection [Monocytes and macrophages remove abnormal and defective RBC, immune function] o Regulation [O2 requirement and metabolic activity, Body temperature, Acid-base balance] o Transportation [Oxygen to cells, CO2 back to lungs, Nutrient transport] • Lymphatic system o Blood filtrations (filters foreign material, reservoir for T&B cells, filters blood and returns back to cardio vascular system • Average lifespan of RBCs 120 days (4 months) • Erythropoietin produced in kidneys o Hormone that stimulates RBC production o Kidneys detect low O2 levels, and hormone is released • Thrombopoietin produced in liver o Hormone that stimulates platelet production • RBC lysis/destruction primarily takes place in the spleen • Males typically have more RBCs due to testosterone, which decreases with age o Women have a high risk of iron-deficiency anemia due to menses |
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S&S of anemia |
• Eyes (yellowing) • Skin (paleness coldness, yellowing) • Respiratory (SOB) • Muscular (weakness) • Intestinal (change in stool colour, bloody/black) • Central (fatigue, dizziness, fainting) • Blood vessels (low BP) • Heart (palpitation, tachycardia, chest pain, angina, heart attack) • Speen (enlargement -> increased RBC destruction) |
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Lab results for anemia testing |
• CBC – Reticulocyte -> developing RBCs • Iron studies (in order of usefulness) o Ferritin (protein that is primary form of iron stored in cells, representative of total amount of iron stored in the body. o Serum iron ( estimate of iron carried in the blood) o Total iron binding capacity (blood’s capacity to bind iron with transferrin, a indirect measure of transferrin) o Transferrin (protein carrying iron in the blood, but can increase when inflammation or infection is present, so is less accurate) |
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Iron deficiency anemia: type of anemia/etiology, causes, risk factors, assessment, S&S |
type: decreased RBC production cause: Nutritional disorder, inadequate iron synthesize Hgb, malabsorption, nutritional deficits, blood loss, hemolysis risk factors: Age, gender (women), diet, culture barriers Assessment: Diagnostic tests • Blood test (Decreased Hct & Hgb, Microcytic, hypochromic) • Diagnostic testing (Stool examination occult blood, colonoscopy, endoscopy, bone marrow) S&S: (more in chronic, asymptomatic early on) o Pallor o Cheilitis (inflammation lips) o Glossitis (Inflammation of tongue) o Headache o Paresthesia o Burning sensation tongue o Lack of iron |
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iron deficiency anemia: Collaborative care and nursing management |
• Ongoing assessment o Cardiorespiratory function, lab values, monitor for bleeding (urine, stool emesis), impact on patient and family • Diet management, medication (oral vs IV iron), malnutrition, alcoholism, replacing iron, o Foods high in iron (nuts, seeds, legumes, egg yolk, dark green veggies, fish and shellfish, lean red meat) • Iron is better absorbed in an acidic environment, take one hour before eating, stomach is most acidic then (ex. alongside vitamin C) • Side effects: constipation, black stools (be careful hemorrhage also causes this) • Iron supplementation teaching o It takes about 2-3 months for change in S&S and lab values after starting to take iron supplements o No enteric coated, with acid/citrus, away from meals o Side effects (heartburn, constipation, diarrhea, black stool, stained teeth, so use straw) • Comfort o Energy conservation, manage pain, limit environment stimulation, teach S&S • Safety o Fall prevention o Medication safety, 10 right o Transfusion safety • Blood transfusions as per MD/NP |
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Thalassemia: type of anemia/etiology, cause, 2 types of thalassemia, |
• Cause: genetic blood disorder, absent/reduced globulin/hemoglobin protein group, reduced RBC production, hemolysis/destruction of RBCs • Minor thalassemia o Microcytosis (small RBCs), hypochromia (pale cells), mild splenomegaly (hypertrophy to break down RBCs), bronze skin colour (deposition of RBC breakdown products in the SC tissue) • Major thalassemia (life-threatening) o S&S of anemia, growth and mental growth effects, splenomegaly, jaundice, hepatomegaly, cardiomyopathy |
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Thalassemia: nursing management |
(for major only, minor does not need treatment) • Blood transfusion • Chelating agent to bind to iron (Folic acid, ascorbic acid, zinc) • Cure: hematopoietic stem cell transplantation |
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Megaloblastic anemias: (pernicious anemia, cobalamin deficiency, folic acid/Vit B12 deficiency, etiology, S&S, Dx) |
• Impaired DNA synthesis resulting in macrocytic RBCs (normochromatic), lifespan of RBCs is shorter, higher chance of hemolysis • Caused by cobalamin and folic acid deficiency, DNA synthesis suppression from medication use • Pernicious anemia o Autoimmune disorder that results in decrease absorption of cobalamin/Vit B12 from the diet (weak stomach absorption, lack of intrinsic factor), Vit 12 deficiency -> megaloblastic anemia o Tx: Vit B12 injection once a month (you need exogenous Vit B12 cuz there’s no intrinsic factor to absorb dietary Vit B12), eating red meat/liver, eggs & dairy • Cobalamin deficiency o Lack of cobalamin in the diet o Gastric mucosa not secreting enough intrinsic factor (reduces absorption) (Disturbance from GI surgery) o Long term use of H2-histamine receptor blockers, causes atrophy or loss of gastric mucosa o Hereditary defects of cobalamin utilization • Folic acid deficiency (aka vit B12) o Folic acid responsible DNA synthesis leading RBC formation and maturation o Result nutritional deficiency, alcoholism • Signs and symptoms o Cobalamin Deficiency [Same as all anemias, GI manifestations, Sore, red, shiny tongue, Anorexia, N&V, Abd pain, Neuromuscular, Weakness, Paresthesia's (feet/hands), Impaired thought process] o Folic Acid Deficiency ‘Same as cobalamine **except NO neurological manifestations** • Diagnosis o Blood smear; RBC large and abnormal shape o Folate level o Decreased B12 levels o Serum anti IF antibody (pernicious anemia) o Serum methylmalonic (MMA), high value in cobalamin deficiency o Serum homocysteine, high in both cobalamin and folic deficiency |
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Megaloblastic anemia: Nursing management |
• Safety (Protect against falls, Burns [decreased pain sensation], Trauma) • Adherence to medication • Administration B12 (IM) if *IF* lacking o 1000 mcg/day (nasal better than injection) • Administration of Folate supplement 1 mg day by mouth • 5 mg/day for malabsorption • Neuro symptoms difficult to reverse • Diet o Cobalamin (red meats, especially liver) o Folic acid (green leafy vegetables, liver, meat, fish . legumes, whole grains) o B6 (meats, wheat germ, legumes, bananas) o Amino acids (meat, milk, milk products..) o Vitamin C (citrus fruits, cantaloupe, strawberries, green vegetables) |
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Megaloblastic anemia: Nursing management |
• Safety (Protect against falls, Burns [decreased pain sensation], Trauma) • Adherence to medication • Administration B12 (IM) if *IF* lacking o 1000 mcg/day (nasal better than injection) • Administration of Folate supplement 1 mg day by mouth • 5 mg/day for malabsorption • Neuro symptoms difficult to reverse • Diet o Cobalamin (red meats, especially liver) o Folic acid (green leafy vegetables, liver, meat, fish . legumes, whole grains) o B6 (meats, wheat germ, legumes, bananas) o Amino acids (meat, milk, milk products..) o Vitamin C (citrus fruits, cantaloupe, strawberries, green vegetables) |
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Aplastic anemia: etiology, causes, diagnosis, S&S |
• Pancytopenia (decreases all blood cell types) • Chronic (manage with erythpoietin or blood transfusion) or critical (manage hemorrhage and sepsis) • Autoimmune condition by autoreactive t lymphocytes, which targe and destroy hematopoietic stem cells • Causes o Idiopathic o Autoimmune o Congenital – Chromosomal alterations o Acquired – Exposure to radiation, chemicals, drugs, viral and bacterial infections • Diagnosis o Decrease Hb, WBC, platelets o Iron and total iron binding capacity elevated sign erythropoiesis suppression • Signs and symptoms o Minor (Fatigue, Dyspnea, Cardiovascular, Pallor, Cerebral response) o Severe (Neutropenia/High risk infection and septic shock, Thrombocytopenia, Risk bleeding) |
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Megaloblastic anemia: Nursing management |
• Safety (Protect against falls, Burns [decreased pain sensation], Trauma) • Adherence to medication • Administration B12 (IM) if *IF* lacking o 1000 mcg/day (nasal better than injection) • Administration of Folate supplement 1 mg day by mouth • 5 mg/day for malabsorption • Neuro symptoms difficult to reverse • Diet o Cobalamin (red meats, especially liver) o Folic acid (green leafy vegetables, liver, meat, fish . legumes, whole grains) o B6 (meats, wheat germ, legumes, bananas) o Amino acids (meat, milk, milk products..) o Vitamin C (citrus fruits, cantaloupe, strawberries, green vegetables) |
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Aplastic anemia: etiology, causes, diagnosis, S&S |
• Pancytopenia (decreases all blood cell types) • Chronic (manage with erythpoietin or blood transfusion) or critical (manage hemorrhage and sepsis) • Autoimmune condition by autoreactive t lymphocytes, which targe and destroy hematopoietic stem cells • Causes o Idiopathic o Autoimmune o Congenital – Chromosomal alterations o Acquired – Exposure to radiation, chemicals, drugs, viral and bacterial infections • Diagnosis o Decrease Hb, WBC, platelets o Iron and total iron binding capacity elevated sign erythropoiesis suppression • Signs and symptoms o Minor (Fatigue, Dyspnea, Cardiovascular, Pallor, Cerebral response) o Severe (Neutropenia/High risk infection and septic shock, Thrombocytopenia, Risk bleeding) |
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Aplastic anemia: nursing management and treatment |
• Treatment o Preventing complications from infection o Treatment options o Bone marrow transplantation o Immuno-suppressive therapy • Management o Identify causative factors o Prevention infection and hemorrhage o Chronic - blood transfusions and erythropoietin o Critical – HSCT (hematopoietic stem cell transplant) and immunosuppressive therapy, corticosteroids |
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Acquired hemolytic anemia: etiology, causes, S&S |
• Causes o Results of hemolysis from physical destruction, immune reactions, infection agents/toxins o Normocytic/Normochromic • Extrinsic factors - Physical destruction, Immune reactions, Infectious agents/toxins • Intrinsic Factors - Hereditary defect of RBC • Signs and symptoms o Jaundice (increased RBC destruction, SOB, fatigue, enlarged spleen and liver, hyperactivity) |
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Acquired hemolytic anemia: etiology, causes, S&S |
• Causes o Results of hemolysis from physical destruction, immune reactions, infection agents/toxins o Normocytic/Normochromic • Extrinsic factors - Physical destruction, Immune reactions, Infectious agents/toxins • Intrinsic Factors - Hereditary defect of RBC • Signs and symptoms o Jaundice (increased RBC destruction, SOB, fatigue, enlarged spleen and liver, hyperactivity) |
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Acquired hemolytic anemia: treatment |
• Treatment o Maintain kidney function (promote hydration, hydration therapy -> Accumulated Hgb can obstruct tubules) |
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Acquired hemolytic anemia: etiology, causes, S&S |
Increased RBC destruction • Causes o Results of hemolysis from physical destruction, immune reactions, infection agents/toxins o Normocytic/Normochromic • Extrinsic factors - Physical destruction, Immune reactions, Infectious agents/toxins • Intrinsic Factors - Hereditary defect of RBC • Signs and symptoms o Jaundice (increased RBC destruction, SOB, fatigue, enlarged spleen and liver, hyperactivity) |
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Acquired hemolytic anemia: etiology, causes, S&S |
Increased RBC destruction • Causes o Results of hemolysis from physical destruction, immune reactions, infection agents/toxins o Normocytic/Normochromic • Extrinsic factors - Physical destruction, Immune reactions, Infectious agents/toxins • Intrinsic Factors - Hereditary defect of RBC • Signs and symptoms o Jaundice (increased RBC destruction, SOB, fatigue, enlarged spleen and liver, hyperactivity) |
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Sickle cell anemia: etiology, treatment, S&S, Dx |
Increased RBC destruction • Autosomal recessive disorder that results in abnormal formation of Hgb in RBC, results in premature destruction, unresolved pain leads to crisis (cells are sticky and can form obstructions, resulting in crisis) • Signs and symptoms o Pain (tachycardia, fever, hypertension, N/V), pallor, jaundice, increased risk for gallstones o Acute chest syndrome (in the heart, lungs, etc), a cause of death o Pain location depends on location, can last a few hours to weeks, spleen is overwhelmed due to high number of damaged RBCs (autospleenectomy) • Diagnostic testing o Peripheral blood smear o CBC o Sickle cell screening test o Hemoglobin electrophoresis o X ray bone and joint deformity o MRI stroke blocked blood vessels o Doppler DVT |
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Sickle cell anemia: nursing management/collaborative care & teaching |
• Nursing and collaborative management o Goals: Alleviate symptoms (pain management), minimize end-target organ damage, treating acute chest syndrome o Collaborative care: pain management, stem cell transplant, preventing infection and fatigue, big temperature changes, transfusion therapy, hydration, oxygen therapy, • Teaching o Minimize ‘triggers’ (high altitudes, temp. extremes, stress, infections, fluid imbalances) o Ongoing screening e.g., retinopathy o Vaccinations (Flu, pneumococcal, etc.) |
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Increased blood loss |
• Nursing management o Stop hemorrhage o Replace blood volume, IV solution, transfusion, iron supplementation, monitor • Acute blood loss o LABS: it takes 2-3 for hemorrhage to be reflected in lab values o 10% loss – vasovagal syncope o 20% loss – no S&S at rest, tachycardia with exertion, slight postural hypotension o 30% loss – tachycardia with exertion, postural hypotension o 40% loss, decrease BP, CVP, CO, reaped/thready pulse, cold diaphoretic skin o 50% loss – lactic acidosis, shock, potential death • Nursing interventions o Monitor labs CBC – reticulocyte Iron studies – serum iron, transferrin, total iron binding capacity (TIBC) Morphological classifications (colour and size) |
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Summary of anemia nursing concerns |
• Activity intolerance o Weakness, malaise, difficulty tolerating increased activity • Imbalanced nutrition o Poor intake, anorexia, weight loss, decreased serum albumin, decreased iron, vitamin deficiency, • Hypoxemia o Decreased hemoglobin |
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Polycythemia: etiology, causes, Dx, S&S, complications |
• Impairs circulation due to increased viscosity and blood volume • Primary polycythemia: JAK2 mutation results in increased sensitivity to erythropoietin receptors resulting in overproduction of RBCs regardless of negative feedback (hypoxic drive) (forms all type of blood components) o Affects males older than 60 more commonly • Secondary polycythemia: pathological, environment causes, overproduction of erythpoietin, compensatory mechanism, etiology – chronic hypoxia, EPO returns to normal once Hgb stabilizes • Diagnosis: o Primary [Low erythropoietin in primary, elevated, Hgb, WBC, Plts, leukocytes, hypercellular RBC, WBC, and plts] o Secondary [increased erythropoietin (EPO)] • Manifestations o Increased blood viscosity, hypertension, pruritis (histamine release), paresthesia (hands//feet), increased risk of blood clotting, headache, vertigo, dizziness • Complications o Thrombosis, stroke, hemorrhage (petechia, ecchymoses, epistaxis, BI bleed), hepatomegaly, splenomegaly |
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Polycythemia: nursing management |
• Phlebotomy (removal of blood), myelosuppressive agent, antiplatelets, allopurinol, Education smoking cessation, Fluid intake and output (prevent fluid overload -> circulatory congestion and underhydration -> increased blood viscosity), Overhydration therapy over Underhydration (dilute the blood/reduce viscosity) • Nutritional assessment (offset inadequate food intake from GI symptoms of feeling full, pain, or dyspepsia/indigestion) • Blood transfusion • Encourage patient activity decrease risk thrombus formation • Active or passive leg exercises and ambulation • For secondary polycythemia, maintain adequate oxygenation and treating the cause of hypoxia |
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Platelets: clotting studies [PT, INR, PTT, aPTT, fibrinogen, D-dimer] |
• Platelet count from CBC • PT Prothrombin Time (PT): is a blood test that measures how long it takes blood to clot (longer, higher = slower clotting = more risk of bleed). It is a measure of factor II (prothrombin) which is synthesized by the liver and is part of the coagulation cascade. It is often used to evaluate the status of patients on warfarin therapy. However, the INR is a more useful indicator and is calculated based on the PT result. • International Normalized Ratio (INR): The normal range for someone not on warfarin is 1.2. However, the target in warfarin therapy is 2-3, which increases to 2.5-3.5 in the case of a valve replacement (depending on the type and location of the valve). Higher = slower clotting. Used as a measurement for warfarin anticoagulant therapy. • Partial thromboplastic Time (PTT): is a blood test that measures the time it takes your blood to clot. Can be used to screen for coagulation deficiencies, and is also useful for monitoring IV heparin therapy (therapeutic range is 60-90 seconds). Higher = longer time to clot = greater risk of bleeding • Activated PTT (aPTT): is considered a more sensitive form of the PTT • Fibrinogen: Fibrinogen is a precursor to fibrin, which is needed to form a fibrin clot. Abnormally low levels of fibrin can result in impaired clotting and increased bleeding risk. Increased fibrinogen may indicate that the patient is hypercoagulable. • D-Dimer: nonspecific test that shows that one or more clots are being broken down somewhere in the body (measure of a DVT or other clot). A number of conditions can cause it to be positive (e.g., DVT, PE, DIC, others). Can be useful in ruling out a DVT or PE in cases where suspicion is low to moderate. |
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Thrombotic thrombocytopenia purpura (TTP): causes, treatment |
• Enhanced agglutination of platelet o Associated hemolytic uremic syndrome o Emergency due to bleeding and clotting • Treatment o Treat underlying disorder (infection) o Plasma exchange o Corticosteroids to suppress splenic macrophages o monoclonal antibody therapy o Immunotherapy |
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Thrombotic thrombocytopenia purpura (TTP): causes, treatment |
• Enhanced agglutination of platelet o Associated hemolytic uremic syndrome o Emergency due to bleeding and clotting • Treatment o Treat underlying disorder (infection) o Plasma exchange o Corticosteroids to suppress splenic macrophages o monoclonal antibody therapy o Immunotherapy |
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Heparin-induced thrombocytopenia: causes, treatment |
• drug-induced (Heparin) • decrease platelets 50% • Leading to bleeding and clotting • Treatment o Discontinue Heparin o Place patient on warfarin once platelet count is high enough |
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Thrombotic thrombocytopenia purpura (TTP): causes, treatment |
• Enhanced agglutination of platelet o Associated hemolytic uremic syndrome o Emergency due to bleeding and clotting • Treatment o Treat underlying disorder (infection) o Plasma exchange o Corticosteroids to suppress splenic macrophages o monoclonal antibody therapy o Immunotherapy |
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Heparin-induced thrombocytopenia: causes, treatment |
• drug-induced (Heparin) • decrease platelets 50% • Leading to bleeding and clotting • Treatment o Discontinue Heparin o Place patient on warfarin once platelet count is high enough |
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Immunologic thrombocytopenia purpura (ITP): causes, treatments, Dx, teaching |
• Abnormal destruction circulating platelets o Autoimmune reaction, Normal platelets, destroyed spleen, survive 1-3 days instead of 8-10 days • Treatment: o Corticosteroids (suppresses splenic macrophages) o Splenectomy (done if body no responding to GCCs) • Diagnostic studies o Platelet levels o Prolonged bleeding occurs o Blood smear • Patient and family teaching o Reduce bleeding risk • Safety alert |
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S&S of bleeding, blood loss |
• Cardiovascular: hypovolemia, ↑HR, ↓ BP, dizziness • Neurological: altered mental status • Gastrointestinal: melena, hematemesis, BRBPR, abdominal pain • Genito-urinary: hematuria, menorrhagia • ENT: gingival bleeding, epistaxis, bleeding of oral mucosa, bullous hemorrhages of the mucosa • Skin: petechiae, purpura, ecchymoses, prolonged bleeding after an injection, hematoma, mucosal bleeding • Wounds/drains: bloody discharge/output • Labs: falling Hb |
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Thrombocytopenia: Patient teaching |
Reducing bleeding risk o Assess medications: antiplatelet meds or anticoagulants? o Humidified oxygen o Gentle nose-blowing o Soft bristle toothbrush, no flossing o Electric razor o Avoid mouthwashes containing alcohol (dries mouth) o Prevent constipation: consider stool softeners o Prevent vomiting: consider antiemetics if nausea o Menstruation: No tampons, track bleeding amount o Avoiding skin tears: consider using Kling bandage as an alternative to adhesive dressing o Assess fall risk, implement individualized and universal strategies o Protective footwear |
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Hemophilia: Cause, S&S, interventions |
o Cause: X-Linked Recessive genetic disorder o Manifestations: slow persistent bleeding from minor cuts, uncontrollable hemorrhage after dental extraction or gingiva irritation, nose bleed after face/head trauma o Nursing interventions: prevent and treat bleeding, replacement therapy (with clotting factors, NOT platelets or steroids), prophylaxis (preventing falls/trauma), treatment of complications and symptoms, prevent moving after trauma to reduce bleeding |
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Van Willebrand’s Disease: cause, S&S, nursing management |
o Cause: congenital bleeding disorder o Manifestation: Uncontrolled bleeding minor injuries, neurological signs: pain, anesthesia, paralysis o Nursing Management: prevent and treat bleeding provide prophylaxis management, lifesaving intervention |
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Van Willebrand’s Disease: cause, S&S, nursing management |
o Cause: congenital bleeding disorder o Manifestation: Uncontrolled bleeding minor injuries, neurological signs: pain, anesthesia, paralysis o Nursing Management: prevent and treat bleeding provide prophylaxis management, lifesaving intervention |
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Disseminated Intravascular Coagulation: etiology, S&S, nursing management |
• Cause: Bleeding and thrombotic disorder o Abnormal response normal clotting cascade, not a disease -> caused by something else o Perfuse bleeding from depletion platelets and clotting factors o Result of predisposing condition Ie. Cancer, acute leukemia, transfusion mismatched blood, liver disease o Cause lots blood clots to form causing ischemia, and other areas to bleed (Too much and too little clotting) • Initiate and accelerate clotting and anticlotting process response disease or injury • Manifestation: Abnormal bleeding and clotting (some bleeding here, some clotting there) • Nursing Intervention: Stabilize bleeding, treat underlying causes, oxygenation/volume replacement, blood products as per MD/NP |
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Neutropenia/low WBC: causes, S&S |
• Neutrophils make up 60% of WBCs (main immune response) o Live about 6-8 hours in the body once released into the bloodstream o ANC is the relation of mature, immature and WBC numbers • Granulocytes • Differential count is the percentage of each type of WBC • Causes o Premature neutrophil destruction (Drug-induced, autoimmune response) o Decrease neutrophil production (Direct bone injury, drugs, nutritional deficiency) Monitoring for S&S of an infection • Mucous membranes of the throat, mouth - Sore throat, dysphagia, ulceration • Skin - Ulcers, wounds • GI - Diarrhea, rectal tenderness • Pulmonary system - Shortness of breath, cough • Genito-urinary -> Urinary frequency, pain -> Vaginal itching or discharge • Change in mental status • Any catheters/tubes can be portals of entry for infection |
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Febrile neutropenia (emergency!): nursing management |
• Febrile neutropenia is present when there is an infection with a decreased/absent ability to fight it • High risk of sepsis, can progress to septic shock • Can be fatal o Sepsis: dysregulated response to infection o Fever or lowered temp (<36°C) o Tachycardia o Tachypnea o Warm, flushed skin in early phrases; cool skin, decreased cap refill, cyanosis, mottling may indicate shock o Altered mental status o oliguria, anuria • Management o Monitor closely for signs and symptoms of sepsis, septic shock o Deterioration can occur rapidly o Identification of the source of infection o Pan cultures: blood, sputum, urine, feces, lesions o Ensure IV access o Rapid initiation of antibiotics o Usually broad-spectrum, IV o The longer the neutropenia, the greater the risk of fungal infection o Antifungals may be prescribed, especially if the fever does not respond to antibiotics o IV fluids |
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Neutropenia w/o fever: management, teaching |
• Management of neutropenia without fever o Carefully assess and monitor for signs and symptoms of infection o Monitor vital signs, especially temperature o Investigation as to underlying cause of the neutropenia o Granulocyte-colony stimulating factor (G-CSF) o May be administered to stimulate bone marrow to increase production of neutrophils • Patient/family teaching o Monitoring for, recognizing signs and symptoms of infection o Monitoring temperature o Avoid Tylenol o Frequent hand hygiene o Avoiding crowds and people who are sick o Do not share food, cups, utensils, toothbrush o Avoid tampons o Shower daily, use lotion to prevent skin from getting dry, cracking o Avoid manicures, pedicures o Avoid handling waste from dogs, cats, other pets (or wear gloves and then wash hands) o Use gloves for gardening or avoid gardening o Don’t go outside barefoot o Foods to avoid (Raw vegetables that have a flower or sprout, Non-pasteurized milk, juices, honey, cheese, Cold cuts, Salad bars, Raw or medium cooked meats, fish, tofu, eggs) |
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Leukaemia: definition, causes, categories |
• Definition: malignant disease affect blood and blood forming tissues: bone marrow, lymph system and spleen • Causes: Genetic and Environmental • Categories: Acute or Chronic |
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Acute lymphocytic leukemia |
• Age: children (2-5), after age 50 • B-cell origin: Immature small lymphocyte proliferate bone marrow • Sign and symptoms o Fever, Weakness, Fatigue, Weight loss, Bleeding tendencies, CNS manifestation |
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Acute lymphocytic leukemia |
• Age: children (2-5), after age 50 • B-cell origin: Immature small lymphocyte proliferate bone marrow • Sign and symptoms o Fever, Weakness, Fatigue, Weight loss, Bleeding tendencies, CNS manifestation |
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Acute myelogenous leukaemia |
• Age: adulthood onset 64 years • Majority leukemia cases • Uncontrolled proliferation myeloblasts (precursors granulocytes) • Sign and symptoms o Fatigue and weakness, Headache, Mouth sores, Fever, Infections |
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Chronic lymphocytic leukemia |
• Age: older adult (50-70 years) • Common western countries • Involve B-Cell • Lymphocyte infiltrate bone marrow, spleen and liver • Lymph node enlargement throughout the body • Sign and symptoms o Early: no S/S o Chronic fatigue, anorexia, splenomegaly and lymphadenopathy and hepatomegaly progress to fever, weight loss fatigue |
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Chronic lymphocytic leukemia |
• Age: older adult (50-70 years) • Common western countries • Involve B-Cell • Lymphocyte infiltrate bone marrow, spleen and liver • Lymph node enlargement throughout the body • Sign and symptoms o Early: no S/S o Chronic fatigue, anorexia, splenomegaly and lymphadenopathy and hepatomegaly progress to fever, weight loss fatigue |
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Chronic myelogenous leukemia |
• Age: older adults • Excess development mature neoplastic granulocytes bone marrow --> infiltrate spleen and liver • Cell cytogenetic abnormalities--> Philadelphia chromosome • Signs and symptoms o Early: no S/S o Progress: fatigue, weakness, fever, weight loss, joint pain, bone pain, splenomegaly, sweating |
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Leukemia: common S&S, Dx, treatment |
• Common S&S o Systemic (weight loss, fever, frequent infection) o Lungs (easy SOB) o Muscular (weakness) o Bones/Joints (pain or tenderness) o Psychological (fatigue, loss of appetite) o Lymph nodes (swelling) o Speen/liver (enlargement o Skin (night sweats, easy bruising and bleeding, purplish patches/spots) • Diagnosis o Peripheral blood evaluation o Lumbar puncture o CT scan • Treatment o Chemotherapy o Corticosteroid o Radiation o Hematopoietic stem cell transplant |
