NUR 211 Unit 5 Clotting Disorders Fall 2024 PDF

Clotting Disorders NUR 211-Fall 2024  Objectives Compare and contrast the pathophysiology, clinical manifestations, and medical/nursing management of the client experiencing clotting disorders. Examine risk factors associated with cellular regulation across the lifespan and the...

Clotting Disorders NUR 211-Fall 2024  Objectives Compare and contrast the pathophysiology, clinical manifestations, and medical/nursing management of the client experiencing clotting disorders. Examine risk factors associated with cellular regulation across the lifespan and the nursing care directed at reducing these risks and provide education on prevention/screenings. Compare and contrast various medications, treatments, blood transfusions, and procedures used to manage disorders involving clotting disorders. Apply the nursing process as a framework to provide age-appropriate, culturally sensitive care of the client experiencing cellular regulation disorders. Develop teaching strategies appropriate to the client. Plan, prioritize, and implement evidence-based nursing care for clients using research and evidence-based practices. Identify therapeutic communication techniques to be used for clients experiencing cellular regulation disorders  Pre-Class Reading  Hemostasis Review Definition: Hemostasis is the process that stops bleeding from a damaged blood vessel. Phases: Vascular Spasm Platelet Plug Formation Coagulation Key Components: Platelets Clotting Factors Fibrin Regulation: Multiple mechanisms exist to ensure the process is tightly regulated, preventing excessive clotting or bleeding. Final Stage: Clot retraction and eventual dissolution (fibrinolysis) once the vessel is healed.  o o THEAlterations o HEART o in Hemostasis o o o o o o Assessment: History oDemographics oMedical oFamily oDiet oSocioeconomic status oCurrent Health Problems  Assessment: Psychosocial o o o o  Assessment: Physical o o o o o o o o Assessment: Diagnostics o o o o o o o o Polycythemia Vera Pathophysiology –  Clinical Manifestations Subjective:  Clinical Manifestations Objective –Mucous membranes –Flushed appearance –Distended veins –Hypertension –Hyperkalemia –Gout-like symptoms –Severe hypoxia –Bleeding issues /spontaneous bleeding  Labs Hemoglobin > 18g/dL in men, >16.5g/dL in women RBC > 6 million/mm^3 Hematocrit > 55%  THE HEART Interventions  Patient Education Hemophilia Hemophilia  ▪ Hemophilia ▪ ▪ ▪ Hemophilia Two common forms: Factor VIII Hemophilia A or Classic Hemophilia Factor IX Hemophilia B or Christmas disease 20,000 people in the US- all races, genders, etc Also has a 3rd form: Von Willebrand Disease (vWD) Hereditary bleeding disorder Characterized by deficiency, abnormality, or abscess of the protein called von Willebrand Factor (vWF).  Deficiency of factor VIII (antihemophilic factor AHF) – Factor VIII Produced in the liver Needed for formation of thromboplastin in phase I of blood Hemophilia A coagulation Individuals with hemophilia had ⅔ of the factors required for coagulation – Vascular influence Pathophysiology – Platelets May bleed for longer periods of time but not at a faster rate Expression varies based on degree of bleeding severity – Severe – Moderate – Mild  – Hemophilia- – Bleeding Expression  Clinical Prolonged bleeding anywhere from or in the body Manifestations Hemorrhage from any trauma: loss of deciduous teeth, circumcision, cuts, epistaxis, injections Excessive bruising, even from slight injury, such as a fall Subcutaneous and intramuscular hemorrhages Hemarthrosis, especially knees, ankles, elbows Hematomas: pain, swelling, limited movement Spontaneous hematuria  Diagnostics Hx of bleeding episodes Evidence of X-linked inheritance Only ⅓ of cases are new mutations DNA testing Laboratory findings Bleeding Time Factor Assays PTT Platelets PT Thrombin Time  Treatment Primary treatment is replacement of missing clotting factors Factor VIII concentrates 1-deamino-8-d-arginine vasopressin (DDAVP) Antifibrinolytic Therapy Tranexamic acid (Cyklokapron) Aggressive factor concentrate replacement therapy is initiated to prevent chronic crippling effects from joint bleeding  Treatment Other drugs may be LESSON CHECK: included depending on the THE HEART source of hemorrhage: o Corticosteroids o Avoid aspirin and traditional NSAIDs o Cyclooxygenase-2 (COX-2) inhibitors, selective NSAIDs o E-aminocaproic acid (Amicar) Complications of Treatment  Treatment Regular exercise and physical therapy Most children are treated at home to prevent delay. Prophylactic therapy w/ periodic replacement Includes factor VIII concentrate infused regularly before the onset of issues Secondary treatment is infusion of factor VIII concentrate AFTER the child has their first joint bleed Treatment centers vary. May be every other day to 3x/week  Prognosis No cure for hemophilia Symptom management With the above, can have an average life expectancy Prior to 1975, pts may have been exposed to HIV Gene therapy may be an option in the future  Bleeding prevention and management Interventions Monitor for signs of bleeding complications Administration of clotting factor replacement therapy Injury prevention and self-care measures Pain management during bleeding episodes Promote physical mobility and joint protection Ensure compliance with treatment plans and medication regimens Educate and support the family Prepare for Home Care Thrombocytopenia  Thrombocytopenia BLOOD VESSELS Reduction of platelets < 150,000 Caused by: Impaired platelet production Increased platelet destruction Abnormal platelet distribution Three types of Thrombocytopenia: o Immune Thrombocytopenia Purpura (ITP) o Thrombotic Thrombocytopenia Purpura (TTP) o Heparin-Induced Thrombocytopenia Purpura (HIT)  Causes of Thrombocytopenia  Specific Pathophysiology Most Common May be autoimmune-related or Usually 5-14 days after starting d/t drug toxicities heparin Usually acute in children, chronic in adults Increase in platelet aggregation Unexplained platelet decrease by >50%, OR decrease in platelets in circulation Decreased platelets Can be fatal Sometimes r/t autoimmune disease  Clinical Manifestations Common for all types:  Clinical Manifestations Small Small microclots block capillaries causing microclots block Presence of tissue ischemia in capillaries major organs antiplatelet Increased risk for causing tissue antibodies in kidney damage, ischemia in major blood myocardial infarction, organs stroke. Increased risk for Venous kidney damage, thromboembolism Pulmonary embolism myocardial Dx made by clinical infarction, stroke. symptoms and history of heparin use  Labs & Diagnostics H&P Bone marrow aspiration/ biopsy CBC and platelets