NCM 112 Midterm Gayatin PDF

LABORATORY AND DIAGNOSTIC TESTS Nursing Implications and Nursing...

LABORATORY AND DIAGNOSTIC TESTS Nursing Implications and Nursing Responsibilities https://assets.newatlas.com/dims4/default/f1b59cd/2147483647/strip/true/crop/5472x3648+0+0/resize/1440x960!/quality/90/?url=http%3A %2F%2Fnewatlas-brightspot.s3.amazonaws.com%2F94%2F4b%2F81c48e4045339d7bf6d6ac9ac363%2Fdepositphotos-100561190-xl-2015.jpg  M: 4.2-5.4 million/mm RBC Count F: 3.6-5.0 million/mm COMPLETE BLOOD M: 14-18 g/dl COUNT Hemoglobin F: 12-16 g/dl DETERMINES PRESENCE OF ANEMIA Hematocrit – F: 37-47% percentage of red cells in total volume of blood M: 45-54%  MCV Mean Corpuscular Volume MCH Mean Corpuscular Hemoglobin MCHC Mean Corpuscular Hemoglobin Concentration https://www.medicine.mcgill.ca/physio/vlab/bloodlab/images/09imag/cytes.jpg  WBC Count 5,000-10,000/cu.mm. COMPLETE Differential Count BLOOD COUNT DETERMINES INFECTION, INFLAMMATION, ALLERGIC Neutrophils/PMN/Segmenters REACTION Basophils Eosinophils Lymphocytes Monocytes Complete Blood Count DETERMINES BLEEDING or THROMBOTIC TENDENCIES Platelet Count 150,000-400,000/cu.mm or (150-400 x 109/L) https://i.pinimg.com/originals/e5/f7/83/e5f7835e3fa0df61f7cf5a7b8e37953f.jpg BONE MARROW ASPIRATION AND BIOPSY – determines defects/abnormalities in blood cell production NURSING RESPONSIBILITIES: Prior to the Procedure Inform patient of physical sensations (e.g. pain, pressure and cold, numbness etc) Describe purpose duration and location Secure consent Procedure Proper Site: Sternum (supine position with small pillow under thoracic spine) or posterior iliac crest (side lying) Patient comfort and support Post Procedure Direct pressure on the site & rest for 30min. BONE MARROW ASPIRATION PROCEDURE Aseptic Technique Anesthesia is applied Short rigid needle with stylet is introduced into the marrow cavity 0.5 – 1 ml of marrow is aspirated Container / slides are labeled properly Length of Procedure: 5-10 https://content.healthwise.net/resources/12.6/en-us/media/medical/hw/h9991531_002.jpg min  Measures the rate in which red blood cells aggregate and sediment at the bottom of a test tube in millimeters per hour. ERYTHROCYTE Increased levels signify presence SEDIMENTATION of infection and inflammatory RATE conditions M= 1-13 mm/hr Normal Range: F=1-20mm/hr https://www.researchgate.net/profile/Vijay_Bhat3/publication/51974320/figure/fig2/AS:601585516290049@15 20440572152/Alkaline-gel-electrophoresis-showing-Lane-1-normal-sample-with-HbA-and-HbA2-Lane-2.png Separates different types of hemoglobin according to their mobility in an electric field HEMOGLOBIN ELECTROPHORESIS  RETICULOCYTE COUNT Are young, non-nucleated erythrocytes Index of bone marrow production of red cells Differentiates anemias caused by bone marrow failure from those cause by hemorrhage or hemolysis Normal range: Adult – 0.5 – 2% https://geiselmed.dartmouth.edu/anatomy/courses/cto/resources/lab9a/images/10.jpg https://images.myupchar.com/4693/iron-test-in-hindi.png Normal Range: 60 – 150 ug/dl Increased: hemolytic disorders, hemochromatosis SERUM IRON Decreased: chronic illness, malignant neoplasms, blood loss, chronic renal disease, extensive burns and iron deficiency anemias (e.g. During pregnancy and rapid growth)  BLOOD TYPING A, B, O, AB Rh TYPE https://s3.amazonaws.com/classconnection/655/flashcards/20681655/jpg/blood_type_test_determines_blood_type_and_compatibility_figure_19___7-16EE2A7C92777F35097-thumb400.jpg  Bleeding time (1-6 min) Clotting time (5-15 min) COAGULATION Prothrombin Time / Protime and INR (12-14 sec) – Partial Thromboplastin Time (60-80 sec) / APTT (30-45 TESTS: determines function of sec) – detects deficiencies in DETERMINES BLEEDING OR clotting factors I, II, V, VII all plasma clotting factors and X except VII, XIII and platelets THROMBOTIC TENDENCIES Thrombin time (10-15 sec) – detects function of the last stage of coagulation DISTURBANCES IN OXYGENATION (HEMATOLOGIC DISORDERS) By: Jonnafe G. Gayatin, RMT, RN, MAN ANATOMY PLASMA – 91.5% water; 8.5% solutes (7% of which are FORMED ELEMENTS: proteins) Electrolytes Red Blood Cells Nutrients White Blood Cells Regulatory substances Platelets Gases Wastes Plasma Proteins  FUNCTIONS OF THE HEMATOLOGIC SYSTEM O2-CO2 Nutrients and wastes TRANSPORTATION Hormones Heat Clotting PROTECTION Phagocytes Antibodies Homeostasis pH REGULATION Temperature Osmotic Pressure  SITE: RED BONE MARROW Tissue Hypoxia triggers hematopoiesis HEMATOPOIETIC GROWTH FACTORS: HEMATOPOIESIS Erythropoietin Colony Stimulating Factors Thrombopoietin Cytokines HEMATOPOIESIS ASSESSMENT Health History - Ethnicity - Family History - Nutritional History - Use of Medications - (Effects of the situation on functional ability, manifestation of distress and coping mechanisms) Physical Assessment: Systems Approach  DIAGNOSTIC TESTS: Blood Count (RBC, WBC, Platelet, Differential Count) Red Blood Cell Indices (MCV, MCH, MCHC) Hematocrit; Reticulocyte Count Coagulation Tests: Protime (INR), aPTT, Clotting Time and Bleeding Time Ferritin Levels Bone Marrow Aspiration and Biopsy  MANAGEMENT Therapeutic Hematopoietic Stem Therapeutic Blood Component Splenectomy Apheresis Cell Transplantation Phlebotomy Therapy Surgical removal of A specific Transplantation of Removal of a Whole blood the spleen component stem cells from certain amount of Packed RBCs Enlarged spleen separated from the either allogenic or blood under Platelets may be the site of blood and removed autologous donors controlled Plasma excessive Usually done to conditions Granulocytes destruction of blood Plateletpheresis patients with severe Usually done to cells aplastic anemia, patients with Lymphocytes Leukapheresis some forms of elevated Cryoprecipitate Erythrocytapheresis leukemia and hematocrits or AHF (Anti- Plasmapheresis thalassemia excessive iron Hemophilic Factor) / Stem Cell Harvest absorption Factor VIII Factor IX Concentrate Factor IX Complex (Factors II, VII, IX, X) Albumin IV Gamma globulin Anti-thrombin III Concentrate HEMATOLOGIC DISORDERS  ANEMIA - – condition wherein hemoglobin concentration is lower than normal ( hemoglobin, rbc count, hematocrit) https://medicine.tamu.edu/class- https://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/styles/wide/public files/histopathology/Histopathology%20Study%20Gui /uploads/images/Microcytic%20hypochromic%20red%20cells%20in%20iron%20deficien de/Hematopoetic-Lymphoid/Slide303Normal15.jpg cy%20anemia.%20Red%20cells%20are%20hypochromic_0.png?itok=ybD4WiW2 CLASSIFICATION OF ANEMIA Defective Production Increased Destruction (Nutritional; Blood Loss (Bleeding) (Hemolytic) Hypoproliferative) Iron Deficiency Trauma Inherited Hemolytic Vitamin B12 Deficiency Bleeding Problems Anemia Folate Deficiency (Epistaxis, Menorrhagia, Abnormal Decreased Bleeding Disorders) Hemoglobin Erythropoietin Blood Cell Membrane Production Abnormality Cancer / Inflammation Acquired Hemolytic Anemia Antibody-Related Not Antibody Related NURSING DIAGNOSIS Inadequate tissue Fatigue r/t decreased perfusion (Oxygen) r/t hemoglobin or decreased oxygen diminished oxygen carrying capacity of the carrying capacity of the blood blood Imbalanced Nutrition: Activity Intolerance r/t Less than body inadequate hemoglobin requirements r/t and hematocrit inadequate intake of essential nutrients Non-compliance with prescribed therapy  https://gizi.unida.gontor.ac.id/wp-content/uploads/2020/04/cegah- anemia-saat-puasa-simasinsurtech-624x260.jpg DEFECTIVE PRODUCTION Nutritional Anemias / Hypoproliferative Anemias Iron Deficiency Vitamin B12 Deficiency Folate Deficiency Decreased Erythropoietin Production Cancer / Inflammation IRON DEFICIENCY ANEMIA Insufficient Dietary Chronic Blood Loss Intake: Pica (craving for (bleeding) unusual substances like ice, clay or laundry starch) Impaired GI absorption Increased Iron (gastrectomy, prolonged requirements (periods of severe diarrhea, intestinal rapid body growth, hookworm infestation, pregnancy, menstruation) bowel diseases) Clinical Manifestations: fatigue, exertional dyspnea Classical Signs: Brittle, spoon- shaped nails with longitudinal ridges (koilonychia); Smooth sore tongue; angular cheilosis (ulceration in the corners of the mouth)  Complete Blood Count DIAGNOSIS Bone Marrow aspiration (definitive) Laboratory Findings: Low hemoglobin Microcytic, hypochromic RBCs Low Serum Iron Concentration High total iron binding capacity (high transferrin levels) low serum ferritin decreased reticulocyte count NURSING MANAGEMENT AND CONSIDERATIONS Administer prescribed iron medication: Iron Preparations: e.g. ferrous sulfate, ferrous gluconate Z-track technique for parenteral. Use straw for liquid oral meds Encourage client to take iron with Vit. C / empty stomach to enhance absorption Educate on foods high in iron (organ meats (beef/chicken liver), cooked white beans (e.g garbanzos), green leafy veggies, raisins, molasses Tannates in tea, carbonates (e.g. softdrinks) and calcium (milk) hinder iron absorption. Stools will be black. Side effect: Constipation. Counsel and instruct high risk clients about preventive education  MEGALOBLASTIC, MACROCYTIC ANEMIAS ▪ Deficiency in vitamin B12 and Folic acid lead to defective DNA synthesis (impaired nuclear development) and abnormal RBC maturation  macrocytic RBCs ▪ Etiology: chemotherapeutic agents, anticonvulsants (interferes with DNA metabolism)  insufficient dietary intake surgery gastrectomy ileal resection malabsorption CAUSES OF pernicious anemia (failure to secrete intrinsic factor) VITAMIN B12 DEFICIENCY CLINICAL MANIFESTATIONS Anemia Beefy Red Tongue Vitiligo Weakness, listlessness, fatigue Neurologic Abnormalities (peripheral neuropathy, loss of balance) Loss of proprioception Mental status changes Impaired memory (Dementia) Depression SIGNS AND SYMPTOMS OF VIT B12 DEFICIENCY https://lh3.googleusercontent.co m/proxy/jFcU3txRJa9DR8L6SQPr QB1u6KoV65Cw- S7JYnzadkQOt6qqdzWJocbEyWg 0yP3vGp4bwF8q7KnbFrpMRdmu nx8lUKkepsYtJLM6F03vjGmSVqx _mAR17pMFqy9HpoKIHxc  Diagnosis: Bone marrow analysis Hyperplasia Pancytopenia macrocytic RBCs (increased MCV) https://i0.wp.com/medicoapps.org/wp- poikilocytosis content/uploads/2019/02/megaloblastic-anemia.jpg?fit=600%2C315&ssl=1  Diagnostic test : Schilling’s Test 24 hour urine sample Management: Vit. B12 Replacement – https://image.slidesharecdn.com/vit-b12-schilling-130316051450- phpapp01/95/vit-b12schilling-4-638.jpg?cb=1363410950 Oral, IM, SQ, intranasal forms Improve thought process minimize effects of paresthesia https://encrypted-tbn0.gstatic.com/images?q=tbn%3AANd9GcSEwf4spw9-gO27sehrlsAKKMpEo_jRyVPO6A&usqp=CAU  Etiology: Dietary deficiency, FOLIC ACID DEFICIENCY chronic alcoholism, overcooking of vegetables, malabsorption syndromes Decreased Folic Acid during pregnancy may lead to Neural Tube Defects (Spina Bifida) Clinical manifestations: anemia macrocytic rbcs (megaloblastic changes in the bone marrow ) decreased serum folate levels https://1.bp.blogspot.com/-Ir1z2jedp9Y/WSxeUqLSnZI/AAAAAAAAGKc/JvblFHHb8QEtr5tmIWR9a_bCWnz47DCJwCLcB/s1600/Folic%2Bacid%2BDeficiency%2BAnemia.jpg MANAGEMENT: oral folic acid supplements; well balanced diet (organ meats, eggs, cabbage, broccoli, citrus fruits, brussel sprouts) 100-200 mg daily HYPROLIFERATIVE ANEMIAS  HYPROLIFERATIVE ANEMIAS Anemias in Renal Disease Anemia of Inflammation -Occurs as a result of kidney damage -Occurs as a result of inflammation, infection and (decreased erythropoietin production) malignancy -Anemia occurs when GFR is less than 30 -Also includes anemia of critical illness and anemia ml/min. associated with aging -Previously known as anemias of chronic disease -Findings: decreased RBC count; normocyctic, normochromic RBCs -Management: treatment of underlying condition  Anemia is related to: mild shortening of rbc lifespan failure of or decreased production of Erythropoietin (EPO) to stimulate RBC production immune activation bone marrow suppression as a side https://www.lalpathlabs.com/blog/wp- content/uploads/2020/02/shutterstock_1120340036-Converted.jpg.png effect of treatment  Clinical Manifestations: Fatigue, Weakness Dyspnea Anorexia Management: Erythropoietin (EPO) Therapy (e.g. Epogen, Procrit, Epoetin alfa) Blood Transfusion https://www.verywellhealth.com/thmb/obSRDJx1HmDYrUDT- G4JTp8U9GY=/3000x2000/filters:no_upscale():max_bytes(150000):strip_icc()/anemia-after-surgery-3156852-Final- 63c258f51d7846e1b24d870a3b8ea88c.png APLASTIC ANEMIA Infection Drugs (antineoplastics, Chloramphenicol, sulfonamides, Phenytoin, radiation chemotherapy) chemicals (benzene and benzene derivatives, pesticides) Depression/ Viruses (Hepatitis B & C, EBV, CMV) Cessation of Miliary TB activity of all blood Fanconi anemia (hereditary) forming elements Decreased RBCs – (Anemia) pallor, fatigue, palpitations, exertional dyspnea Markedly reduced Decreased WBCs – (Granulocytopenia) susceptibility to infection hematopoiesis Decreased Platelets – (Thrombocytopenia) hemorrhage/bleeding (bone marrow aplasia) MANAGEMENT Removal of the Causative Agent Blood Transfusion Bone Marrow Transfusion with HLA Compatible donor Monitor and manage infection and bleeding DISTURBANCES IN OXYGENATION: HEMATOLOGIC DISORDERS PART 2: Hemolytic Anemias (Anemias of Increased Destruction) INHERITED HEMOLYTIC ANEMIAS Abnormal Hemoglobin Sickle Cell Disease Thalassemia Enzyme Deficiency G6PD Deficiency Blood Cell Membrane Abnormality Acanthocytosis Hereditary Elliptocytosis Hereditary Spherocytosis Stomatocytosis https://www.hopkinsmedicine.org/-/media/images/health/1_- conditions/heart-and-vascular/hemolytic-anemia-teaser-image.ashx SICKLE CELL ANEMIA An autosomal codominant inherited disease Abnormal hemoglobin (HbS) Sickle shaped RBCs Globin fraction abnormality – valine is substituted for glutamic acid in the 6th position of the beta chain Sickle Cell Trait (heterozygous) Sickle Cell Disease (homozygous) Sickle cells have a shortened life span of 7-20 days and is Trivia: Sickle Cell Gene offers a protective destroyed by the spleen effect against Plasmodium spp.  Pathophysiology OXYGEN TENSION DECREASES HbS POLYMERIZES RBC BECOMES SICKLE SHAPE INCREASED BLOOD VISCOSITY/ PROLONGED CIRCULATION TIME/ISCHEMIA CNS: THROMBOSIS/CVA, PARALYSIS, HEPATIC: HEPATOMEGALY, GALL STONES CEREBRAL DEFICITS, DEATH CARDIAC: SYSTOLIC MURMUR, SKELETAL: DACTYLITIS, DEFORMITIES, CARDIOMEGALY, HEART FAILURE/MI OSTEOMYELITIS, OSTEOPOROSIS, FRACTURES RESPI: ACUTE CHEST SYNDROME, GENITAL: PENAL PRIAPISM HYPERTENSION, PNEUMONIA RENAL: HEMATURIA, RENAL FAILURE OPTIC: HEMORRHAGE, RETINOPATHY, BLINDNESS SPLEEN: SPLENOMEGALY, SPLENIC ATROPHY DERMIS: STASIS ULCERS https://3.bp.blogspot.com/_ZWqgY BROGHw/TRkTQY4714I/AAAAAAA ACEA/P7k3L-vNCQQ/w1200-h630- p-k-no-nu/17.jpg  ▪ Three Types: Causes of Crisis: ▪ Vaso-occlusive crisis stress ▪ Aplastic Crisis dehydration ▪ Splenic Sequestration crisis change in oxygen tension in the body ▪ Others: infection ▪ Infectious crisis fever SICKLE CELL ▪ bone, joint and other crisis anesthesia CRISIS ▪ Megaloblastic Crisis over-exertion exposure to cold high altitudes ▪ Two major consequences of high hemoglobin levels rbc sickling: ingestion of alcohol ▪ Chronic Hemolytic Anemia smoking ▪ Blood Vessel Occlusion  https://static01.nyt.com /images/2019/12/07/sci ence/07SICKLECELL1/07S ICKLECELL1- ASSESSMENT & DIAGNOSIS mobileMasterAt3x.jpg Monitor for: Heart Failure https://www.microscopyu.com/assets/gallery- images/pathology_sicklec ellanemia40x02.jpg Fluid Retention Neurologic: Paresthesia, confusion, balance Diagnostic Tests: Screening: Metabisulfite Test (Sickling Test/Sickledex) Confirmatory: Hemoglobin Electrophoresis MANAGEMENT Hydroxyurea Erythropoietin Supplemental Iron, Folic Acid and Vitamin B12 Antibiotics Opioids (Morphine – drug of choice) Antihistamines, NSAIDS Hydration Pain Management O2 Therapy Frequent Transfusions Bone Marrow Transplantation Genetic Counseling Diet: increased CHON, calcium, https://science.sciencemag.org/content/sci/367/6483/1198/F1.large.jpg?width=800&height=600&carousel=1 vitamins and adequate liquids  NURSING MANAGEMENT Manage Pain Manage Fatigue Prevent / Manage Infection Antibiotics and Wound Care Promote Coping Skills Patient Education (Minimize Knowledge Deficit) Hydroxyurea is teratogenic Monitor and Manage Potential Complications Home and Community Based Care https://i.pinimg.com/originals/27/52/32/275232dad5a25489826b1a257a7ea688.jpg  https://i.ytimg.com/vi/o1YubvuTISY/maxresdefault.jpg THALASSEMIA A diverse group of genetic disorder characterized by a primary, quantitative reduction in globin chain synthesis for hemoglobin. Homozygous – Thalassemia Major (Disease) Heterozygous – Thalassemia Minor (Trait) – milder forms Types: Alpha Thalassemia – Barts Hydrops Fetalis, Hb H disease, Constant Spring disease, Silent Carrier Beta Thalassemia – Cooley’s Anemia, Hb Lepore https://www.stepwards.com/wp-content/uploads/2016/01/05_21gProteinHemoglobin-L.jpg PATHOPHYSIOLOGY defective hemoglobin chain synthesis imbalance in hemoglobin configuration precipitates in the erythroid precursors increased rigidity premature destruction of the rbc/ hemolysis in the spleen MANIFESTATIONS Hydrops Fetalis marked skeletal deformities (frontal bossing); cheek bone and jaw protrusions DIAGNOSIS AND MANAGEMENT Diagnostic Findings: Hypochromia and microcytosis, hemolysis Splenomegaly Management: Blood Transfusions; Bone Marrow Transplantation (for patients https://www.stepwards.com/wp-content/uploads/2016/01/img0028.jpg under 5 yrs. old); Splenectomy Consent Pre-Op teaching Monitor for Hemorrhage Prevent pneumonia and atelectasis Monitor platelet count (elevated first 2 weeks) https://www.limamemorial.org/TransAdam/doc/graphics/images/en/17212.jpg INHERITED HEMOLYTIC ANEMIAS Abnormal Hemoglobin Sickle Cell Disease Thalassemia Enzyme Deficiency G6PD Deficiency Blood Cell Membrane Abnormality Acanthocytosis Hereditary Elliptocytosis Hereditary Spherocytosis Stomatocytosis https://www.hopkinsmedicine.org/-/media/images/health/1_- conditions/heart-and-vascular/hemolytic-anemia-teaser-image.ashx  G6PD DEFICIENCY X-linked inherited disease (ENZYME DEFICIENCY Common in African and ANEMIA) Mediterranean Descents https://i.pinimg.com/originals/ 5b/7c/5d/5b7c 5d80780b1be5 726de14cb8ed ed0a.jpg https://images.medindia.net/patientinfo/950_400/symptoms-of-g6pd-deficiency.jpg  Pathophysiology of G6PD Deficiency Deficiency in G6PD enzyme that metabolizes glucose and generate ATP decreased GSH (glutathione) oxidative denaturation of hemoglobin (Methemoglobin) formation of Heinz bodies increased cell rigidity lysis in the spleen MANAGEMENT Recognition of the disorder (Newborn Screening) Avoidance/Cessation of offending substances Hydration Blood transfusion Prompt treatment of infection https://pbs.twimg.com/media/D5gRdY6WAAEcVVe.jpg https://sites.google.com/site/livestrongwithg6pddeficiency/_/rsrc/14 93450217924/website-builder/G6PDD_Prohibited%20items.png Blood Cell Membrane Abnormalities HEREDITARY SPHEROCYTOSIS Autosomal Dominant genetic disorder Alteration in the shape of erythrocytes characterized by a membrane abnormality that leads to osmotic swelling of the RBCs. Manifestations: Anemia – pallor, fatigue, dyspnea Jaundice splenomegaly https://image.slidesharecdn.com/haem14-hemolyticcongenital-150415203434-conversion-gate02/95/haem14- hemolytic-anemia-congenital-4-638.jpg?cb=1429148140  DIAGNOSIS AND MANAGEMENT DIAGNOSIS MANAGEMENT: -Diagnostic Test: Chromium -Splenectomy Survival -Cholecystectomy (due -Laboratory Findings: to increased incidence Increased Osmotic Fragility (Erythrocyte of gall stones) Fragility Test) -Genetic Counseling Increased Reticulocyte count -Energy Conservation Increased Bilirubin Techniques  OTHERS: (Research Work) Hereditary Stomatocytosis Acanthocytosis Elliptocytosis  ACQUIRED HEMOLYTIC ANEMIA Antibody Related Not Antibody Related Autoimmune Hemolytic Anemia Disseminated Intravascular Coagulation Iso-Antibody/Transfusion Reaction Hypersplenism Cold Agglutinin Disease Infection Liver Disease Mechanical Heart Valve Microangiopathic hemolytic anemia Paroxysmal Nocturnal hemoglobinuria Toxins Trauma Uremia IMMUNE MEDIATED HEMOLYTIC ANEMIAS Types of Immune Mediated Antibodies: Autoantibodies – produced by a person in response to drugs and disease Alloantibodies – comes from an exogenous source Classifications of autoantibodies: Warm Reacting Cold Reacting Acquired HEMOLYTIC ANEMIA Causes: chemicals, EXPOSURE HEMOLYSIS OF RBCS toxins, venom, infections (malaria) SIGNS AND SYMPTOMS OF ANEMIA  Warm Reacting Autoimmune Hemolytic Anemia usually idiopathic or may ANTIBODIES (IgG/IgA) ACT ON RBCS AT TEMP 37C UP be associated with SLE, RA, Chronic Lymphocytic Leukemia and myeloma ANTIBODIES REACT WITH ANTIGENS ON RBC MEMBRANE DESTRUCTIVE MEMBRANE CHANGES (SPHEROCYTOSIS) RBC HEMOLYSIS IN THE SPLEEN Cold Reacting Autoimmune Hemolytic Anemia ANTIBODIES (IgM) REACT WITH RBC ANTIGENS AT Etiology: Raynaud’s TEMP 31C BELOW disease, Infectious Mononucleosis, ACTIVATION OF Mycoplasma COMPLEMENT SYSTEM Pneumoniae infection, EBV, mumps and SOME CELLS CLUMP HEMOLYSIS Legionnaire’s Disease IN CAPILLARY BEDS VASCULAR OBSTRUCTION CYANOSIS, PAIN, PARESTHESIA Drug Induced Hemolytic Anemia Reaction to drugs (e.g. Methyldopa, penicillin, quinine and quinidine) production of autoantibody destruction of erythrocyte (HEMOLYSIS) Manifestations  DIAGNOSIS: Positive Coomb’s Test (antiglobulin test) decreased hematocrit increased reticulocyte count increased bilirubin MANAGEMENT Immunosuppressive Agents [cyclophosphamide (Cytoxan) or azathioprine (Imuran)] Corticosteroids (Cyclomen) Splenectomy Blood Transfusions Plasmapheresis Teach patient about drug therapy Avoid exposure to cold (for patients with cold reacting anemias) Help patient cope with illness  OTHER BLOOD DISORDERS AND COAGULATION DISORDERS https://www.aniara.com/mm5/graphics/00000001/Blog/coagulation.jpg  Primary: ERYTHROCYTOSIS Polycythemia Vera Secondary: hypoxia (high altitudes, renal cell CA, pulmonary and cardiac diseases) caused by excessive production of erythropoietin https://d16qt3wv6xm098.cloudfront.net/avqJLJ-zQcyrPghkq4s9jcB8Sga4X0wj/_.jpg  https://calgaryguide.ucalgary.ca/wp- content/uploads/2015/05/Polycythmia-Vera.jpg  CLINICAL MANIFESTATIONS: (due to hypervolemia and increased blood https://boneandspine.com/wp-content/uploads/2010/02/erythromelalgia.jpg viscosity) - headache, vertigo, tinnitus, blurred vision, fatigue, red or ruddy itchy skin, dyspnea, angina, claudications, thrombophlebitis, hepatomegaly, splenomegaly Pruritus – histamine release by increased number of basophils Erythromelalgia – burning sensation in fingers and toes  Complications Thrombosis, Gout, Acute Leukemia, Emboli, Myelofibrosis https://post.healthline.com/wp-content/uploads/2020/07/484811-Polycythemia-Vera-Self-Care-from-Head-to-Toe-12996x2855-Body.png MANAGEMENT Nursing Diagnosis Ineffective Tissue Perfusion r/t hyperviscosity of the blood Medical Management: Phlebotomy, radioactive phosphorus and interferon, hydration to decrease blood viscosity Hydroxyurea – suppress bone marrow function allupurinol (Zyloprim) for increased uric acid levels dipyridamole (Persantine) for ischemic symptoms anagrelide (Agrylin); Aspirin– helps prevent thrombosis Nursing Interventions: (Symptomatic management) Encourage ambulation, avoid long periods of rest Adequate hydration  DISORDERS ASSOCIATED WITH PLATELETS AND COAGULATION https://transfusionnews.com/wp-content/uploads/2019/11/TRF11062019-GettyImages-1088373948-1.jpg  EXTRINSIC INTRINSIC PATHWAY PATHWAY COMMON PATHWAY Natural Anticoagulants: Anti- Heparin Thrombin III Protein C Protein S  Thrombocytosis – increased number of platelets Thrombocytopenia – decreased Terms: number of platelets Coagulation Disorders - Bleeding syndromes THROMBOTIC Also known as DISORDERS HYPERCOAGULABILITY hemostasis in exaggerated forms and predisposes to thrombosis. Causes: increased platelet number and/or function increased clotting activity  THROMBOCYTOSIS (Increased number of platelets) Secondary: due to disease and Primary: due to genetic other conditions (e.g. chronic condition (e.g Primary inflammatory disorders, iron thrombocythemia in cases of deficiency, malignant disease, polycythemia vera) acute hemorrhage, and splenectomy  Causes of increased platelet function: atherosclerotic plaques, Increased smoking, increased lipids, hemodynamic stress, Diabetes Platelet Mellitus and immune mechanisms. Function Vessel Damage  Platelet Adherence  Thrombosis INCREASED CLOTTING ACTIVITY: Hereditary Disorders (PRIMARY) Mutations in Factor V gene and Prothrombin Gene = LEIDEN MUTATION Factor Va cannot be inactivated by protein C = antithrombotic counter regulatory mechanism is lost Protein C Deficiency Hyperhomocystinemia Anti-thrombin III deficiency Protein S deficiency INCREASED CLOTTING Stasis due to prolonged bed rest, immobilization, MI, CA, hyper- ACTIVITY: estrogenic states, oral Acquired contraceptives, smoking and Thrombophilia obesity (SECONDARY) Anti-phospholipid Syndrome – antibodies directed against phospholipids binding proteins that function as anticoagulants. ANTICOAGULANT THERAPY Enhances AT III and inhibits platelet function APTT-Maintain at 1.5-2.5x the control Heparin Therapy Complication: Heparin Induced Thrombocytopenia (HIT) Give IV or SQ never IM; Antidote: Protamine sulfate Low Molecular Special form with more selective effect on coagulation Weight Heparin Has longer half life Less incidence of HIT Therapy Warfarin / Vitamin K antagonist / interferes with synthesis of Vit. K dependent clotting factors (II, VII, IX, X) Coumadin Therapeutic range: INR 2.0-3.0 Therapy Antidote: Vitamin K NURSING FOCUS: Management for Thrombotic Disorders Avoid activities that promotes circulatory stasis (immobility, crossing legs etc.) Avoid smoking Ambulation and range of motion exercises Prophylactic anticoagulants (low strength aspirin) Administration of prescribed anticoagulants https://cdn.clipart.email/a8667ccbea62014dd03ecfbd52e31d47_nursing-is-a-work-of-heart-clipart_750-1000.jpeg  BLEEDING DISORDERS Causes: Deficient platelets Decreased Platelet activity Deficient clotting factors https://static01.nyt.com/images/2018/04/22/magazine/22mag-tip/22mag-22tip-t_CA0-superJumbo.jpg THROMBOCYTOPENIA lower than normal number of circulating platelets. More common in women May result from: Decreased platelet production Decreased platelet survival Increased platelet destruction Sequestration of blood in the spleen Consumption of platelets Loss from hemorrhage IDIOPATHIC THROMBOCYTOPENIC PURPURA Etiology: unknown (some may suspect viral infections in children, sulfa drugs, SLE, or pregnancy) Antiplatelet antibodies that bind to platelets are found in blood of patients with ITP Clinical manifestations: Petechiae, ecchymoses, purpura, hypermenorrhea, epistaxis, gingival bleeding https://bloodspecialistclinic.com/wp-content/uploads/2015/03/Thrombocytopenia-e1433829294708-600x409.jpg  corticosteroids, Oncovin/ immunoglobulin Vincristine therapy, (chemotherapy), Treatments splenectomy, Anti-D (WinRho); for ITP: immunosuppressive Plasma Exchange, drugs (Prednisone, Transfusion with cyclophosphamide, platelet azathioprine, concentrates dexamethasone, Danazol), * ⚫PossibleEtiology: Genetics, RA, SLE, Sarcoidosis; also associated with ⚫lymphoma, pregnancy, bacterial endocarditis and drugs ⚫(sulfonamides, penicillin, oral contraceptives, cyclosporine. THROMBOSIS DEPLETION OF PLATELETS fever w/o infection, anemia, nausea, anorexia, weakness, petechiae and hematuria HEMOPHILIA hereditary coagulation disorder characterized by deficient or impaired clotting factors Hemophilia A – Factor VIII Deficiency – a sex linked disorder transmitted on an x- chromosome by carrier women to their sons Hemophilia B – Factor IX Deficiency – also known as the Christmas Disease – sex linked recessive trait Hemophilia C – Factor XI Deficiency  an autosomal dominant trait disorder VON described by Eric von Willebrand in 1926 WILLEBRAND’S associated with defects in both Factor DISEASE VIII:C and the Von Willebrand Factor (VIIIR:Ag)  Clinical Manifestations of Hemophilia: history of lifelong bleeding tendency repeated episodes of spontaneous bleeding into joints excessive bleeding after dental extractions life threatening hemorrhages(retroperitoneal, intracranial and peritracheal soft tissue bleeding) Laboratory Findings: Prolonged PTT but normal platelet count and Protime Treatment: Replacement of Aminocaproic Desmopressin deficient Local treatment Acid (Amicar) (DDAVP) coagulation factor fresh or frozen a fibrinolytic icebags, manual synthetic plasma, enzyme pressure or vasopressin cryoprecipitate, inhibitor can dressings, analog, Factor VIII slow down immobilization, administered concentrate dissolution of elevation, nasally, induces clones clots topical a transient rise (Recombinate anticoagulants in factor VIII and Kogenate) (fibrin foam and levels thrombin) (RICE)  Management Avoid Control Prevent Encourage Avoid injury and Control Bleeding Prevent Joint Encourage Self-care possible bleeding Episodes Degeneration Medic alert Tag safety RICE Immobilize Avoid overprotecting Epistaxis: sit up and Passive to Active ROM Regular Treatment (e.g lean slightly forward Avoid prolonged schooling) immobility Nursing Considerations: EDUCATE MEDIC ALERT PAIN CONTROL LIFESTYLE GENETIC PATIENT TAG: NAME, MODIFICATIONS COUNSELING REGARDING BLOOD TYPE, DISEASE PHYSICIAN’S CONDITION NAME AND DISORDER  VITAMIN K DEFICIENCY Etiology: decreased dietary intake, treatment with neomycin Vitamin K is a cofactor in the Source: 50% of vitamin K is sulfate, intake of drugs (coumarin synthesis of clotting factors II, VII, obtained from normal diet; 50% derivatives, salicylates, quinine IX and X is produced by intestinal bacteria and barbiturates), interference with absorption (Crohn’s disease, ulcerative colitis) Treatment: Oral or Parenteral Laboratory Findings: prolonged Vitamin K preparations Protime (PT) and PTT, Decreased (menadione, phytonadione); Vit. K dependent clotting factors Fresh frozen Plasma  a response of the body’s hemostatic mechanisms characterized by a complicated and potentially fatal process characterized first by clotting and secondarily by hemorrhages. DISSEMINATED INTRAVASCULAR DIC is essentially an imbalance between the process of coagulation and anticoagulation COAGULATION Possible Precipitating Factors leading to DIC: sepsis, anoxia, burns, snake bites (venom), obstetric complications, cancer, toxins, hemolytic transfusion reactions, shock, anaphylaxis  Precipitating Factors Initiation of clotting process Aggregation of platelets and formation of fibrin clots Continuation of Start of fibrinolysis Clotting process Formation of fibrin Depletion of platelets Degradation products and Clotting factors Acts as anticoagulants BLEEDING  Clinical Manifestations: bleeding, petechiae, ecchymosis, hypoxia, tachypnea, hemoptysis, dyspnea, cyanosis, decreased level of consciousness, hypotension, acidosis, and fever Laboratory findings: abnormal RBCs, increased fibrin degradation products, prolonged thrombin time https://healthjade.net/wp-content/uploads/2019/12/DIC.jpg  Management: treatment of the primary disease improving oxygenation and fluid replacement Blood Transfusion – FFP, Platelet concentrates, cryoprecipitates, fresh whole blood Heparin Therapy* Special Nursing Considerations: Record amount and nature of drainage Observation of new bleeding sites Maintaining fluid balance – adequate hydration Monitor for signs of fluid overload during blood transfusions Monitor urine output Family support GENERAL NURSING MANAGEMENT FOR PATIENTS WITH BLEEDING DISORDERS  HEMATURIA NOSEBLEEDS COMMON SIGNS GINGIVAL BLEEDING BRUISING HYPOTENSION BLEEDING PRECAUTIONS https://i.pinimg.com/originals/92/05/28/920528f17a149347f3dec2ef06584a34.jpg FLUIDS AND ELECTROLYTES Part 1 Jonnafe G. Gayatin, RMT, RN, MAN  FLUID COMPARTMENTS: INTRACELLULAR (2/3) Basic EXTRACELLULAR (1/3) Concepts Intravascular Interstitial Transcellular – cerebrospinal, pericardial, synovial, intraocular, pleural fluids, sweat and digestive secretions  Loss of ECF into a space that does not contribute to the equilibrium between the ICF and ECF Third Space Occurs in ascites, burns, peritonitis, bowel Fluid Shift obstruction, massive bleeding into a joint or body cavity (Third Spacing) S/S: (Intravascular Fluid Volume Deficit) – increased HR, decreased BP, decreased CVP, Decreased Urine Output edema, increased weight, Intake and Output Imbalance Electrolytes MAJOR CATIONS (+) MAJOR ANIONS (-) Sodium (ECF) Chloride (ECF) Potassium (ICF) Bicarbonates Calcium Phosphates (ICF) Magnesium (ICF) Sulfates Hydrogen Proteinates  MAJOR ELECTROLYTES INSIDE THE CELL POTASSIUM – 3.5-5.0 PHOSPHORUS – 2.5-4.5 MAGNESIUM – 1.5-2.5 mEq/L mg/dl mEq/L Dominant ICF Cation Major ICF Anion ICF Cation Regulates cell Promotes energy Regulates excitability storage; carbohydrates, neuromuscular Conduction of nerve fat and CHON contraction impulse metabolism Promotes normal Muscle contraction and Acts as hydrogen buffer functioning of nervous myocardial membrane Key role in and cardiovascular responsiveness mineralization of bones system Controls ICF osmolality and teeth Aids in CHON synthesis, Na and K ion Transportation  MAJOR ELECTROLYTES OUTSIDE THE CELL SODIUM – 135-145 CHLORIDE – 96-106 CALCIUM – 8.6-10.2 BICARBONATE – 22- mEq/L mEq/L mg/dl 26 mEq/l Major ECF Cation Major ECF Anion Stabilizes cell Regulates acid- Regulates fluid Helps maintain membrane and base balance volume in the ECF normal ECF reduces its Helps govern ECF osmolality permeability to osmolality Affects body pH; sodium Maintains plasma vital role in acid- Transmits nerve volume base balance impulses; contracts muscles, Activates nerve coagulate blood and muscle cells Form bones and teeth  Regulation of Body Fluid Compartments Osmosis Osmotic Pressure – amount of hydrostatic pressure needed to stop the flow of water by osmosis. Determined by concentration of solutes. Oncotic Pressure – osmotic pressure exerted by proteins (e.g. albumin) Osmotic Diuresis – increase in urine output caused by the excretion of substances such as glucose, mannitol or contrast agents in the urine Diffusion Filtration Sodium – Potassium Pump Source: https://i.pinimg.com/736x/73/ab/cf/73abcf3787f060366b2d3643e4321a3b.jpg Figure 3.11 Operation of the sodium-potassium pump, a solute pump. Slide 1 Extracellular fluid Na+ Na+ K+ Na+-K+ pump Na+ Na+ Na+ K+ Pi Pi Na+ K+ ATP Na+ 1 2 3 K+ ADP 1 Binding of cytoplasmic Na+ 2 The shape change expels 3 Loss of phosphate restores to the pump protein stimulates Na+ to the outside. Extracellular the original shape of the pump phosphorylation by ATP, which K+ binds, causing release of the protein. K+ is released to the causes the pump protein to inorganic phosphate group. cytoplasm, and Na+ sites are change its shape. ready to bind Na+ again; the cycle repeats. Cytoplasm  Normal Urine Output Kidneys = 1ml / kg / hr Routes of Skin Sweat – approx. 600ml / day Fluid Gains and Losses Lungs Breathing - approx. 400 ml/day GI Tract 100-200 ml /day Source: https://img.brainkart.com/imagebk32/HL4gK4E.jpg Evaluating Fluid Status Osmolality Number of solutes per kilogram of solvent Osmolarity Number of particles of solute per liter of solution Measures the ability of the kidneys to excrete or conserve water Urine Specific Gravity 1.010 – 1.025 (1.003-1.030) End-product of protein metabolism BUN 10 – 20 mg/dl End product of muscle metabolism (NV: 0.7-1.4 mg/dl) Creatinine Best indicator of renal function Volume percentage of RBCs (NV = M: 42-52% ; F:35-47%) Hematocrit Increased in dehydration and polycythemia; Decreased in overhydration and anemia Urine Sodium Sodium and Water go together HOMEOSTATIC MECHANISMS HOMEOSTATIC MECHANISMS Kidney Functions Regulation of ECF volume and osmolality by selective retention and excretion of body fluids Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of unneeded substances Regulation of pH in the ECF by retention of hydrogen ions Excretion of metabolic wastes and toxic substance Heart and Blood Vessel Functions – circulation Lung Functions – breathing Pituitary Functions – ADH Adrenal Functions – Aldosterone and Cortisol Parathyroid Functions – PTH (calcium and phosphate Balance)  Baroreceptors Low Pressure baroreceptors – Left Atria High Pressure baroreceptors – Nerve endings in the aortic arch, carotid sinus and afferent arteriole of the nephron Renin-Angiotensin-Aldosterone System Antidiuretic Hormone (ADH) and Thirst Mechanism HOMEOSTATIC MECHANISMS Most significant factor in determining concentration of urine Osmoreceptors Located on the surface of the hypothalamus Senses changes in sodium concentration and release impulses to the posterior pituitary for the release of ADH Atrial Natriuretic Peptide (Atrial Natriuretic Factor) Released by muscle cells of atria of the heart. Action is opposite of RAA System. Released in response to increased arterial pressure, Angiotensin II stimulation, endothelin and sympathetic stimulation Effect: Decreased blood pressure and blood volume Source: https://cdn.britannica.com/21/185321-050-9EA74796/Renin-angiotensin-system.jpg  ANP / ANF Function Source: https://www.cvphysiology.com/uploads/images/anp.png FLUID VOLUME DISTUBANCES FLUID VOLUME DEFICIT FLUID VOLUME EXCESS  FLUID VOLUME DEFICIT (HYPOVOLEMIA) Occurs when loss of ECF volume exceeds the intake of fluid. Water and Electrolytes are lost in the same proportion as they exist in normal body fluids. May occur alone or in combination with other imbalances Note: The term DEHYDRATION refers to loss of water alone. Common Causes: decreased intake, vomiting, diarrhea, GI suctioning, sweating Risk Factors: Diabetes Insipidus, adrenal insufficiency, osmotic diuresis, hemorrhage, coma Other causes: Third Space Shifts – edema in burns, ascites in liver dysfunction https://images.slideplayer.com/25/8077456/slides/slide_20.jpg Clinical Manifestations and Assessment Findings Oliguria; Decreased skin Postural Weight loss concentrated turgor hypotension urine Flattened neck Cool clammy Increased Weak rapid HR veins, decreased skin; peripheral temperature CVP vasoconstriction Muscle Anorexia; Lassitude Thirst Weakness; Nausea (Weakness) Cramps  Increased Hematocrit Increased BUN; increased (Decreased hct and hgb urine specific gravity in Hemorrhage) Diagnostic Hypokalemia with GI and Hyperkalemia with Findings renal losses adrenal insufficiency (Addison’s disease) Hypernatremia results Hyponatremia occurs from increased insensible with increased thirst and loss and Diabetes ADH release Insipidus (decreased urine specific gravity) Medical and Nursing Management Correction of Fluid Loss Monitor: Intake and Output, weight, vital signs, CVP, Level of consciousness, breath sounds, skin/tongue turgor Check Urine concentration Prevent FVD: control measures and oral fluid replacement of losses Correcting FVD: Oral Fluids, ORESOL, IV Fluid replacement https://d16qt3wv6xm098.cloudfront.net/YfG4YPomS-WMzAqveomW2b_WRpey6qjG/_.png  ISOTONIC IV SOLUTIONS ISOTONIC IV SOLUTIONS REMARKS 0.9% NaCl (Normal Saline) Expands ECF Only solution that may be administered with blood products Lactated Ringer’s Solution Contains electrolytes at same concentration as those in plasma Used in treatment of hypovolemia, burns, fluids lost in diarrhea, acute blood loss replacement Should not be used in lactic acidosis and renal failure 5% Dextrose in Water Isotonic solution that supplies 170 cal/L and free water to aid in renal excretion of solutes  OTHER IV SOLUTIONS HYPOTONIC REMARKS Used to treat hypertonic dehydration, Na and Cl depletion and gastric 0.45% NaCl fluid loss NOT indicated for 3rd Space Shifts and Increased ICP HYPERTONIC REMARKS Used in Increased ECF Volume; to decreased cellular swelling; assists 3% NaCl in removing intracellular fluid excess 5% NaCl Used to treat symptomatic hyponatremia; cautious administration COLLOID REMARKS Dextran in NS or Volume/plasma expander; used to treat hypovolemia in early shock D5W Decreases red blood cell coagulation https://i.pinimg.com/originals/ 4c/6b/61/4c6b61701816db0e7 50dfbf3c59139d8.jpg FLUID VOLUME EXCESS (HYPERVOLEMIA) Isotonic expansion of the ECF caused by ETIOLOGY: abnormal retention of water and sodium; Serum sodium concentration may remain * simple fluid overload; diminished function essentially normal. of homeostatic mechanisms responsible for regulating fluid balance *Heart failure, renal failure, cirrhosis of the liver, low protein intake, anemia *Consumption of excessive amounts of table salt or other sodium salts *Excessive administration of sodium- containing fluids. CLINICAL MANIFESTATIONS Crackles, Distended neck Edema shortness of Tachycardia veins breath, wheezing Increased BP, Increased urine pulse pressure Increased weight output and CVP DIAGNOSTIC FINDINGS DECREASED BUN AND DECREASED SERUM XRAY – PULMONARY HEMATOCRIT OSMOLALITY CONGESTION MEDICAL MANAGEMENT Symptomatic Dietary restriction of sodium Diuretics Hemodialysis or peritoneal dialysis  NURSING MANAGEMENT Preventing, Detecting and Monitor: Controlling Fluid Volume Managing Edema: Excess: Intake and Output, Promoting rest, Treating the cause weight, breath sounds, restricting sodium Diuretic therapy degree of edema intake, proper Restriction of Fluids and positioning, adherence Sodium to treatment Elevation of Extremities Application of Elastic compression stockings Paracentesis; Dialysis Continuous renal replacement therapy https://qph.cf2.quoracdn.net /main-qimg- 161740f53480b8e71e9d25a 9aef2b9f6-pjlq  FLUID AND ELECTROLYTE IMBALANCES Part 2 Jonnafe G. Gayatin, RMT, RN, MAN ELECTROLYTE IMBALANCES  HYPONATREMIA HYPERNATREMIA HYPOKALEMIA HYPERKALEMIA HYPOCALCEMIA ELECTROLYTE HYPERCALCEMIA IMBALANCES HYPOMAGNESEMIA HYPERMAGNESEMIA HYPOPHOSPHATEMIA HYPERPHOSPHATEMIA HYPOCHLOREMIA HYPERCHLOREMIA SODIUM IMBALANCES Hypernatremia Hyponatremia  HYPONATREMIA Serum Sodium below 135 mEq/L Loss of Sodium Vomiting, diarrhea, fistulas, diuretics, adrenal insufficiency (aldosterone deficiency) Gain of Water / Water Intoxication (Dilutional Hyponatremia) Syndrome of Inappropriate ADH secretion (SIADH), hyperglycemia, electrolyte- poor parenteral fluids, tap water enemas / irrigations, compulsive water drinking (psychogenic polydipsia)  Headache, lethargy, Anorexia, nausea, dizziness, confusion, vomiting seizure CLINICAL Muscle cramps, Papilledema, dry MANIFESTATIONS weakness, muscle skin, edema twitching of Hyponatremia: Labs: decreased Increased pulse, serum and urine decreased BP, sodium, decreased weight gain, edema urine specific gravity and osmolality  Sodium Replacement Oral, NGT or parenteral (Lactated Ringer’s, NSS) (hypertonic solutions 3% or 5% NaCl if with neurologic symptoms) For SIADH – hypertonic saline with diuretic; lithium or demeclocycline MEDICAL Note: serum sodium must not be increased by MANAGEMENT more than 12 mEq/L in 24 hours to avoid neurologic damage due to osmotic demyelination. Overcorrection can cause lesions in the pons. Fluids are administered slowly and in small volumes. Water Restriction Far safer than sodium administration  Promote early detection and treatment Monitor Intake and Output and Body Weight Note abnormal losses of sodium or gains of water Monitor CNS signs and symptoms Elderly patients are at risk for hyponatremia due to changes in renal functions and decreased ability to excrete excessive NURSING water. MANAGEMENT Encourage foods with high sodium content. Administer hypertonic sodium fluids cautiously especially those with cardiovascular disease. Assess for signs of circulatory overload. For patients taking lithium, monitor for toxicity (N: 0.8-1.2 mEq/L) Monitor serum and urine sodium levels  Serum Sodium Levels exceeding 145 mEq/L Patient loses more water than sodium or patient ingests or retains more sodium than water. Causes: HYPERNATREMIA Fluid deprivation (e.g. unconscious, very old, very young, cognitively impaired) Hypertonic enteral feedings without adequate water Watery diarrhea, greatly increased insensible water loss Diabetes Insipidus Heat stroke, near-drowning in sea water Malfunction in dialysis proportioning systems IV administration of hypertonic saline solutions; excessive use of sodium bicarbonate  (results from cellular Thirst dehydration) CLINICAL MANIFESTATIONS Moderate: restlessness and Severe: disorientation, weakness delusions, hallucinations Dry swollen tongue, sticky mucous membranes, flushed LABS: serum sodium >145 skin, peripheral and mEq/L; serum osmolality pulmonary edema, postural >300 mmol/L; increased urine hypotension, increased specific gravity and muscle tone and deep tendon osmolality reflexes MEDICAL MANAGEMENT Infusion of hypotonic Desmopressin electrolyte solution (DDAVP) to treat (0.3% NaCl) or an diabetes insipidus if it isotonic non-saline is the cause of solution (e.g. D5W) hypernatremia NURSING MANAGEMENT Check fluid gains and Obtain medication history Check for thirst losses Monitor changes in Preventing behavior (restlessness, Monitor temperature Hypernatremia: ensure disorientation, adequate water intake lethargy) Correcting Hypernatremia: monitor IV infusions, sodium levels and neurologic s/s (Note: too rapid reduction can cause cerebral edema) https://www.nurseb uff.com/wp- content/uploads/201 4/09/hypernatremia- signs-and-symptoms- nursing- mnemonics.jpg POTASSIUM IMBALANCES NV: 3.5-5 mEq/L Remember: Potassium influences both skeletal and cardiac muscle activity  Causes: Inadequate intake – elderly, alcoholism, anorexia GI Losses – diarrhea, vomiting, gastric suctioning Use of Diuretics HYPOKALEMIA Alterations in Acid Base Balance – Alkalosis : Hypokalemia Hyperaldosteronism – increases renal potassium wasting Magnesium depletion causes renal potassium loss (correct Mg first) Theophylline Toxicity  Fatigue, muscle weakness Dysrhythmias, increased sensitivity to digitalis ECG: Flat / Inverted T waves; depressed ST segments; Elevated U wave Anorexia, nausea, vomiting Leg cramps, paresthesia Manifestations: Decreased bowel motility Severe hypokalemia – cardiac and respiratory arrest Prolonged hypokalemia – inability to concentrate urine (polyuria, nocturia) ; excessive thirst Potassium depletion depresses release of insulin } glucose intolerance Source: https://www.registerednursern.com/wp-content/uploads/2016/01/hypokalemia- mnemonic-nclex-nursing-electrolytes.png  MEDICAL / NURSING MANAGEMENT: Increase dietary intake Oral / IV replacement therapy (40-80 mEq/day) Monitor urine output Do not exceed 20 mEq/100ml dilution at rate 10-20 mEq/hr Administer using IV Infusion pump, DO NOT GIVE as IV PUSH OR IM!!! Monitor ECG and ABG and Renal Function Prevention: adequate intake, avoid abuse of laxatives or diuretics  Less common but more dangerous Causes: Blood hemolysis during collection can cause pseudo- hyperkalemia Marked leukocytosis and thrombocytosis Administration of Aged / Stored Blood in patients with HYPERKALEMIA impaired renal function Decreased renal excretion in untreated renal failure Hypoaldosteronism – sodium loss and potassium retention Taking KCl, heparin, ACE Inhibitors, captopril, NSAIDS and Potassium-Sparing Diuretics Acidosis : Hyperkalemia (as H goes in the cell; K goes out) Lysis of malignant cells post chemotherapy CLINICAL MANIFESTATIONS Cardiac: early - peaked T-waves, ST depression, shortened QT interval; then – prolonged PR; P Muscle weakness, paralysis waves disappear; later – (peripheral nervous system) prolongation of the QRS complex. VENTRICULAR DYSRHYTHMIAS and CARDIAC ARREST GI: nausea, intestinal colic, diarrhea Source: https://www.registerednursern.com/wp-content/uploads/2016/01/hyperkalema-nclex-nursing-labs.png  MEDICAL MANAGEMENT: Restriction of Cat-ion Emergency IV IV Loop Diuretics Peritoneal dietary exchange management: administration administration Dialysis; potassium and resins Calcium of Sodium of Regular hemodialysis potassium (KAYEXALATE) Gluconate Bicarbonate Insulin and containing except in Hypertonic Monitor BP and medications patients with Dextrose ECG (bradycardia is paralytic ileus indication to stop Solution infusion) Caution in patients taking digitalis  NURSING MANAGEMENT: Observe Monitor Avoid Careful Caution Observe for Monitor Avoid prolonged Careful Caution patients muscle laboratory tests torniquet administration of on potassium weakness, and ECG application IV treatments; rich foods and dysrhythmias, during blood Mix KCl well potassium paresthesia, extraction. when containing nausea, incorporating in medications intestinal colic IV solution especially if with renal dysfunction  CALCIUM IMBALANCES CALCIUM BALANCE Vitamin D Parathyroid Calcitonin Estrogen and Calcitriol Hormone Note: CALCIUM is inversely proportional with PHOSPHORUS!!!  Serum Calcium below 8.6 mg/dl Causes: Elderly, prolonged bed rest Hypoparathyroidism ( decreased PTH) Massive administration of citrated blood Pancreatitis HYPOCALCEMIA Renal failure (hyperphosphatemia) Inadequate Vit. D, magnesium deficiency, medullary thyroid carcinoma, low serum albumin, alkalosis and alcohol abuse Medications that can cause hypocalcemia: aluminum containing antacids, aminoglycosides, caffeine, cisplatin, corticosteroids, mithramycin, phosphates, isoniazid and loop diuretics CLINICAL MANIFESTATIONS Chvostek’s Sign – Tetany – increased Trousseau’s Sign – twitching of muscles neural excitability; Tingling, Spasms carpal spasm supplied by the facial Hyperactive DTR nerve Seizures, depression, Hyperactive bowel ECG – prolonged QT impaired memory, Dyspnea and sounds, dry and interval, Torsades de confusion, delirium, Laryngospasms brittle hair and nails, Pointes hallucinations abnormal clotting Osteoporosis https://i.pinimg.com/originals/2 1/0a/5e/210a5e5b3d4cc82332c ce2eebb911264.png  REMEMBER! Source: https://scontent.fceb1-2.fna.fbcdn.net/v/t1.6435-9/96722245_1541712566031044_7352294921904062464_n.jpg?stp=dst-jpg_p180x540&_nc_cat=110&ccb=1- 7&_nc_sid=8bfeb9&_nc_ohc=Sfenbh18j5kAX8KGIy5&_nc_ht=scontent.fceb1-2.fna&oh=00_AT_RZNR8oXa4_MvoyPPSxocM_SMt9RIv09AklL3Ne5ZLQA&oe=6351F901  IV administration of calcium (calcium gluconate, calcium chloride, calcium gluceptate) MEDICAL MANAGEMENT Medications: alendronate (Fosamax), residronate (Actonel), raloxifene (Evista), calcitonin and ibandronate (Boniva)  Careful administration of IV calcium Too rapid – can cause cardiac arrest! ; slow IV bolus or infusion (diluted in D5W) IV calcium has same effect with digitalis = can lead to digitalis toxicity in those with digitalis therapy Extravasation can cause cellulitis and necrosis of tissues Never mix with saline, phosphate or bicarbonate solutions NURSING Seizure precautions; monitor airway MANAGEMENT Patient education: Dietary intake Adequate exercise; Caution for falls for those with osteoporosis Compliance with medications Avoid overuse of laxatives and antacids  Dangerous when severe (50% mortality) Causes: malignancies; hyperparathyroidism Immobilization HYPERCALCEMIA Thiazide diuretics Milk-alkali syndrome Vitamin A and D intoxication, Use of Lithium  Reduced neuromuscular excitability: muscle weakness, incoordination, anorexia, constipation Digitalis toxicity is aggravated by hypercalcemia Excessive urination due to disturbed tubular function; severe thirst CLINICAL Confusion, impaired memory, slurred speech, MANIFESTATIONS lethargy, acute psychotic behavior, coma Chronic HyperCa+ – increased secretion of acid and pepsin = PUD Hypercalcemic crisis: Cardiac standstill at calcium levels of 18 mg/dl and above, severe thirst and polyuria, intractable nausea, obstipation or diarrhea MEDICAL MANAGEMENT Administration of fluids (0.9% NaCl) and Restricting dietary Furosemide = IV Phosphate calcium Increasing renal excretion IV phosphate therapy – Calcitonin (IM) – from Biphosphonates – (caution: can cause salmon; check for inhibit osteoclast severe calcification of allergy activity tissues)  Encourage fluids; increase mobility Note: Sodium favors calcium excretion NURSING MANAGEMENT Safety precautions of neuro s/s are present Monitor cardiac rate and rhythm and ECG (premature ventricular contractions, paroxysmal atrial tachycardia and heart block) MAGNESIUM IMBALANCES  HYPOMAGNESEMIA Ionized fraction of Mg Magnesium levels should Mg levels less than 1.3 involved in neuromuscular be evaluated in mEq/L and other physiologic combination with albumin activity is measured levels Usually overlooked. Can occur in alcohol Meds that can cause withdrawal, administration hypoMg: aminoglycosides, Causes: NGT suctioning, of TPN, Diabetic cyclosporine, cisplatin, diarrhea, fistulas Ketoacidosis treatment, diuretics, digitalis, and rapid administration of amphotericin citrated blood  Neuromuscular: hyperexcitability (increased DTR) with muscle weakness, tremors, athetoid movements, tetany, seizures, other s/s of accompanying hypocalcemia ECG changes: prolonged QRS, depressed ST, PVC, supraventricular Manifestations: tachycardia, torsades de pointes Prone to digitalis toxicity Alterations in mood, apathy, depression, apprehension, extreme agitation, ataxia, dizziness, insomnia, confusion Delirium, auditory / visual hallucinations, frank psychoses https://i0.wp.com/emcrit.org/wp-content/uploads/2019/08/mglevelinterel.jpg?resize=575%2C232&ssl=1  MEDICAL MANAGEMENT: Mild hypomagnesemia – Intake of Magnesium Rich Foods (green leafy Side effect of excessive ingestion - vegetables, diarrhea nuts/seeds/legumes, whole grains, seafood, cocoa) Magnesium sulfate IV – via Monitor vital signs infusion pump (not to Monitor Mg levels exceed 150mg/min) Antidote: Calcium gluconate  Monitor for digitalis toxicity Seizure precautions for severe hypomagnesemia NURSING Check ability to swallow MANAGEMENT Assess Deep Tendon Reflexes Patient Education: Avoid abuse of diuretics, laxatives and alcohol Teach about magnesium rich foods  Rare Most common cause – Renal Failure False results: hemolyzed specimen, prolonged/tight torniquet application Also seen in patients with untreated diabetic ketoacidosis HYPERMAGNESEMIA Can occur in excessive administration of magnesium to treat PIH. Other causes: Addison’s disease, hypothermia, abuse of laxatives, opioids and anticholinergics, decreased elimination due intestinal hypomotility CLINICAL MANIFESTATIONS Nausea, vomiting Depressed CNS and Decreased BP due to weakness, soft tissue PNS activity – peripheral calcifications, facial decreased Deep vasodilation flushing, sensations Tendon Reflexes of warmth Lethargy, difficulty Above 10mEq/L = speaking Coma, AV block and depression of (dysarthria), cardiac arrest respiratory center drowsiness  Avoid administration of magnesium to patients with renal failure Monitor critical patients under magnesium therapy MEDICAL In emergencies – ventilatory support and MANAGEMENT: calcium gluconate administration Hemodialysis with a magnesium-free dialysate Loop diuretics + NSS or PLR enhances Mg excretion  Monitor vital signs (especially hypotension Monitor and shallow respiration) NURSING Observe Observe DTR and level of consciousness MANAGEMENT: Caution Caution in administering magnesium therapy especially in patients with renal failure https://cdn.pi cmonic.com/ pages/wp- content/uplo ads/2019/04/ Magnesemia- Hypo-vs- Hyper-v2.png