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59 Cards in this Set
- Front
- Back
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Hemolytic Anemia
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Destruction or hemolysis of RBCs at rate > production
3rd major cause anemia Intrinsic- RBC defective- abnormal hemoglobin, enzyme deficiencies, RBC membrane abnormalities Extrinisic- factor other than erythrocytes Jaundice sometimes acute tubular necrosis |
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Sickle Cell Disease
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Group of inherited, autosomal recessive disorders- both genes req
Presence of abnormal form Hb in erythrocyte (HbS)- sub valine for glutamic acid on beta globin chain of Hb Hbs causes RBC to stiffen & elongate d/t dec O2 levels Incurable, often fatal Triggers during high stress- sick, cold, dehydrated, fever |
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Normal vs. Sickle Hb
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Normal: disk-shaped, soft, easily flow through sm bl vessels, lives 120days
Sickle: sickle-shape, hard, often get stuck in sm bl vessels, live 20days or less |
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Sickle Cell Disease CM
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asymptomatic except during sickling episodes
sickle cell crisis is vasoocclusive s/s: pain & swelling of joints, pallor of mucous membranes, fatigue |
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Sickle Cell Anemia Treatment
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supportive care- pain mgmt, O2 for hypoxia & control of sickling, IV hydration, antibiotics
Hydroxyurea prevent sickling Prevention of crisis Transfusion if necessary Stem cell transplantation Renal/ pulmonary failure *Don't give Demerol- causes seizures- life threatening |
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Polycythemia
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Vera: neoplastic transformation hematopoietic stem cells
Secondary: chronic hypoxemia Results in inc bl viscosity & risk of thrombi- inc coagulability, myloproliferative Trt- removal of cause, phlebotomy, bone marrow suppressants CM: hypervolemia & hypervisosity cause symptom, HTN- HA, vertigo, dizziness, tinnitus, visual disturbances, bl vessel distention, impaired bl flow, thrombosis & tissue hypoxia-> paresthesias & CV symptoms Plethora, hyperuricemia, gen pruritus- exacerbated by heat At risk for stroke & hemorrhage |
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Polycythemia Treatment
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Goal: reduce bl vol & viscosity
Phlebotomy dec Hct to <48%, IV hydration, secondary- avoid hypoxia Monitor I/O, nutritional status Anti-thrombus activities- ambulate, plexi pulses, coumadin, heparin |
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Hydroxyurea
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suppresses bone marrow
Polycythemia treatment |
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Interferon
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lowers blood counts
Polycythemia |
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Anegrelide
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dec platelets
Polycythemia |
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Hemolytic Anemia
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Destruction or hemolysis of RBCs at rate > production
3rd major cause anemia Intrinsic- RBC defective- abnormal hemoglobin, enzyme deficiencies, RBC membrane abnormalities Extrinisic- factor other than erythrocytes Jaundice sometimes acute tubular necrosis |
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Sickle Cell Disease
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Group of inherited, autosomal recessive disorders- both genes req
Presence of abnormal form Hb in erythrocyte (HbS)- sub valine for glutamic acid on beta globin chain of Hb Hbs causes RBC to stiffen & elongate d/t dec O2 levels Incurable, often fatal Triggers during high stress- sick, cold, dehydrated, fever |
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Normal vs. Sickle Hb
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Normal: disk-shaped, soft, easily flow through sm bl vessels, lives 120days
Sickle: sickle-shape, hard, often get stuck in sm bl vessels, live 20days or less |
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Sickle Cell Disease CM
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asymptomatic except during sickling episodes
sickle cell crisis is vasoocclusive s/s: pain & swelling of joints, pallor of mucous membranes, fatigue |
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Sickle Cell Anemia Treatment
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supportive care- pain mgmt, O2 for hypoxia & control of sickling, IV hydration, antibiotics
Hydroxyurea prevent sickling Prevention of crisis Transfusion if necessary Stem cell transplantation Renal/ pulmonary failure *Don't give Demerol- causes seizures- life threatening |
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Polycythemia
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Vera: neoplastic transformation hematopoietic stem cells
Secondary: chronic hypoxemia Results in inc bl viscosity & risk of thrombi- inc coagulability, myloproliferative Trt- removal of cause, phlebotomy, bone marrow suppressants CM: hypervolemia & hypervisosity cause symptom, HTN- HA, vertigo, dizziness, tinnitus, visual disturbances, bl vessel distention, impaired bl flow, thrombosis & tissue hypoxia-> paresthesias & CV symptoms Plethora, hyperuricemia, gen pruritus- exacerbated by heat At risk for stroke & hemorrhage |
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Polycythemia Treatment
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Goal: reduce bl vol & viscosity
Phlebotomy dec Hct to <48%, IV hydration, secondary- avoid hypoxia Monitor I/O, nutritional status Anti-thrombus activities- ambulate, plexi pulses, coumadin, heparin |
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Hydroxyurea
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suppresses bone marrow
Polycythemia treatment |
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Interferon
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lowers blood counts
Polycythemia |
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Anegrelide
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dec platelets
Polycythemia |
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ANC calculation
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WBC x (% segs + %bands)
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Neutropenia
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Reduction in neutrophils- most common WBC, phagocytosis
Dx: WBC count, ANC ANC < 1000-1500/ul Severe < 500ul Inc risk of infection- pathogenic as well as normal flora |
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Neutropenia s/s
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Inflammatory response not so responsive
Fever = infection = respond! Minor infections -> sepsis-> septic shock Watch for c/o sore throat, dysphagia, nonproductive cough, lesions, diarrhea, perirectal discomfort |
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Neutropenia nursing management
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Antibiotic therapy prophylactic, empiric (broad spectrum till determine problem), or therapeutic
Growth factor improvement: G-CSF (Neupogen): stim neutrophil production IV or SubQ only- GI destroys; cause bone pain, too much causes leukocytosis Infection control, monitor s/s infection, cultures Avoid invasive procedures Consider thrombocytopenia Protect the pt! |
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Leukemia
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group malignant disorders affecting blood & blood-forming tissues of bone marrow, lymph sys, spleen
Occurs all age groups Accumulation dysfunctional cells d/t loss regulation in cell division Fatal if untreated No single causative agent Assoc factors: chem agents, chemotherapeutic agents, viruses, radiation, immunologic deficiencies |
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Leukemia Classifications
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Acute: clonal proliferation of immature hematopoietic cells
Chronic: mature WBC, gradual onset 4 types: Acute Lymphocytic, acute myelogenous, chronic myelogenous, chronic lymphocytic |
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Acute Myelogenous Leukemia (AML)
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25% all leukemias (85% acute leukemias in adults)
Abrupt, dramatic onset- serious infections/ abnormal bleeding Uncontrolled proliferation myeloblasts Hyperplasia of bone marrow Too many granulocytes AML young cells/blasts d/t too many granulocytes Treat: chemo, radiation, bone marrow transplant |
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Acute Lymphocytic Leukemia (ALL)
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Most common type in children
Immature lymphocytes proliferate in bone marrow s/s abrupt: fever w no obvious cause, bleeding, black marks, aches in arms & legs, enlarged lymphnodes, HA, petechiae, prolonged bleeding from minor scrapes, tired a lot, vomiting CNS manifestations common High survival rate AKA lymphoblastic leukemia Remission easy as adults |
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Chronic Myelogenous Leukemia (CML)
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Excessive mature neoplastic granulocytes in bone marrow- move into peripheral bl in massive #s, ultimately infiltrate liver & spleen
Philadelphia chromosome** disease specific marker Chronic, stable phase- followed by acute, aggressive (blastic) phase, lasts several yrs; pt may only live short time after dx |
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Chronic Lymphocytic Leukemia (CLL)
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Production & accumulation of functionally inactive but long-lived mature-appearing B-lymphocytes
Lymph node enlargement present throughout body- inc incidence infection Complications from early-stage CLL rare- develop as disease advances; pain, paralysis from pressure caused by enlarged lymph nodes Most common leukemia in adults |
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Leukemia CM
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Usually related to bone marrow failure- overcrowding by abnormal cells, inadequate production normal marrow elements
Inadequate marrow elements-> anemia, thrombocytopenia, dec # & function of WBCs Cells cause- splenomegaly, hepatomegaly, lymphadenopathy, bone pain, joint pain, meningeal irritation, oral lesions, solid masses |
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Leukemia dx studies
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To dx & classify: Peripheral blood evaluation, bone marrow evaluation
To ID cell subtype & stage: morphologic, histochemical, immunologic, & cytogenic methods; CT & lumbar punctures to see extent of disease |
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Leukemia Treatment
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Chemo is mainstay treatment
Monoclonal antibodies: use genetic tech to target & kill CA cells, antibody binds to known antigen on surface of lymphocyte, antibody-antigen complex is destroyed by immune sys Stem cell transplantation- eradicate pt own cells then replace w HLA matched cells Combo drugs to: dec drug resistance, min toxicity, & interrupt cell mutation |
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Hodgkin's Lymphoma
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CA originates in lymphocytes
Reed-sternberg cells: lg cell, multi nucleated, insidious, lg non-tender lymphnodes EBV, genetics, exposure to toxins, inc in HIV CM: enlarged lymph nodes, wt loss, fatigue, weakness, tachycardia, night sweats, pruritis, alcohol, cough, dyspnea, stridor, liver & spleen enlargement 2x men than women |
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Hodgkin's Lymphoma diagnostics
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Blood analysis
Biopsy- definitive Bone marrow exams- staging Radiologic exam- CT, MRI, PET, for staging Noted- leukopenia & thrombocytopenia, hyopferremia, hypercalcemia, hypoalbumineria |
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Non-Hodgkin's Lymphoma
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Indolent vs. rapidly developing
unknown cause More common in immunosuppressed No hallmark cell = non-Hodgkin's CM: unpredictable, painless lymph node enlargement, s/s relative to location Dx: similar to Hodgkin's, MRI, BE |
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Lymphoma nursing management
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Chemotherapy care, radiation therapy care, pancytopenia, pain control, aware of type/ involvement- specifically for NHL; psychosocial & spiritual support
Focus on: infection, hemorrhage, & fatigue if bone marrow suppression from chemo |
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Multiple myeloma
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CA plasma cells invade bone marrow & destroy bone
AKA plasma cell myeloma CA cells produce abnormal & excessive amt antibodies & cytokines Insufficient normal plasma cells reduces immune fxn Skeletal pain is most common presenting symptom Cause unknown 2x men than women, Af Amer Overgrowth plasma cells -> bone, bone marrow, kidneys, spleen, cardiac CM: bone pain exacerbated by mvmt, osteoporosis, pathologic bone fractures, hypercalcemia, myeloma protein can cause renal failure, anemia, thrombocytopenia, neutropenia |
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Multiple myeloma dx studies
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Proteins secreted from malignant plasma cells can be detected in urine- M antibody protein, Bence-Jones protein
Radiologic studies reveal lytic bone lesions Bone marrow analysis reveals lg #s plasma cells |
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Multiple Myeloma Treatment
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Rarely cured, goal is remission & relief of symptoms
Chemo Corticosteroids for anti-tumor action & dec swelling Biological therapy Hematological Stem Cell Transplant Mgmt hypercalcemia & prevention of pathologic bone fractures are important components of therapy Analgesics for pain mgmt Radiation to make more comfortable Bi-phosphates to keep bone from breaking done quickly & help w hypercalcemia Lasix to flush Ca, also give K Priorities: Hydration, pain mgmt, safety (weak bones) |
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Thrombocytopenia
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Immune & non-immune causes
Immune thrombocytopenic purpura (ITP): platelets become coated w antibodies, macrophages in spleen destroy platelets (only last 1-3days), most commonly acquired autoimmune disease CM: Bleeding- mucosal, cutaneous (ecchymoses, petechiae, purpura), prolonged bleeding time, risk high for catastrophic hemorrhage |
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Thrombocytopenia Diagnostics
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Platelet count < 150,000/ ul
< 50,000/ul prolongs bleeding time, < 20,000/ul at risk for spontaneous hemorrhage Coagulation studies may indicate which part coagulation cascade is involved- PT, aPTT Bone Marrow studies- ensure not d/t anemia |
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Thrombocytopenia Collaborative care
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Dependent on etiology
Steroids inhibit antibody formation, beef-up capillaries, keep macrophages from killing, splenectomy- option not 1st choice |
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Blood Therapy Indications
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Restore intravascular volume
Restore oxygen carrying capacity of blood Replace clotting factors &/or platelets Replace WBCs |
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Whole Blood
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Replace RBC mass & plasma volume
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Packed RBC
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Preferred method of replacing RBC mass
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Leuko-poor RBCs
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Replaces RBC's while preventing febrile, non-hemolytic transfusion rxn
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Irradiated RBCs
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Replaces RBC's while preventing graft vs host disease
Used in immunocompromised cts |
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Fresh Frozen Plasma
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Replaces plasma w/o RBC's or platelets
Contains most coagulation factors Used in control of bleeding |
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CAUTION
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7 warning signs of CA
C-hange in bowel/bladder habit A- sore that doesn't heal U-nusual bleeding/discharge T-hickening/ lumps I-ndigestion/dysphagia O-bvious change in wart/ mole N-agging cough or hoarsness |
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Factors of CA treatment modality
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Cell type, location & size tumor, extent of disease (how far gone- localized or metastasized), physiologic & psych status, expressed needs & desires
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Classification of CA
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Anatomic site
Histology (tissue of origin)- grading severity, embryonal ectoderm (skin & gland), endoderm (resp tract, GI, GU), sarcoma (embryonal mesoderm- connective tissue, muscles, fat), lymphomas & leukemias (hematopoietic sys) Extent of disease- staging |
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CA grade classification
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Grade 1- mild dysplasia- cells differ slightly from normal,well differentiated
Grade 2- moderate dysplasia- cells more abnormal & mod differentiated Grade 3- severe dysplasia- cells very abnormal & poorly differentiated Grade 4- anaplasia, worst prognosis bc undifferentiated- cells immature & primitive, cell of origin difficult to determine Grade w histology |
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CA Staging Classifications
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After dx, before treatment
0: CA in situ 1: Tumor limited to tissue of origin, localized tumor growth 2: limited local spread 3: Extensive local & regional spread 4: Metastasis |
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TNM CA classification
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For solid tumors
Done at beginning & throughout disease RTNM- restaging Anatomic extent of disease based on 3 parameters: T- Tumor size & invasiveness N- spread of lymph nodes M- metastasis |
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Collaborative Care of CA
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Curative therapy- surgery alone or periods of systemic therapy
Control treatment- initial course & maintenance therapy Palliation goal- relief or control of symptoms, maintain quality of life, good prognostic indicators- sm tumor size, clean tissue margins, absence lymph node involvement Palliative procedures- debulking of tumor or radiation therapy to relieve pain or pressure, colostomy for bowel obstruction, laminectomy for relief spinal cord compression |
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Chemotherapy
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use of chemicals as systemic therapy for CA
goal: reduce # malignant cells in tumor site Standard for most solid tumors & hematologic CA Routes- oral, IM, IV, intracavitary, intrafecally, intraarterially, subQ, topically Various perfusions Drugs may be irritants or vesicants Agents can't distinguish b/w normal & CA cells Body's response to products of cell destruction- acute, delayed, or chronic Acute toxicity SE: dysrhythmias, n/v, alopecia, skin rash, alt bowel fxn, cummulative neurotoxicity |
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Interleukin II (proleukin)
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Chemotherapy
SE: insomnia, SOB (indicates pulmonary edema), generalized aches, dec appetite |
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Common SE of chemo & radiation
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bone marrow suppression, fatigue, GI disturbances, integumentary & mucosal rxns, pulmonary effects, reproductive effects
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