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66 Cards in this Set
- Front
- Back
Can you have inflammation without infection?
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Yes, but you can't have infection without inflammation
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Inflammation
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sequential respone to cell injury, neutralizes and dilutes inflammatory agent, removes necrotic materials, establishes an enviroment suitable for healing and repair
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Local S and Sx of inflammation
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redness, heat, pain, swelling, loss of function
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Systemic response to inflammation
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Increased WBC count with a Shift to the left, malaise, nausea, and anorexia, increased pulse and respiratory rate, fever
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Nursing interventions for inflammation?
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Acute intervention for fever: antipyretics, RICE, Health Promotion, keep wound if present clean and bandaged.
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What is Viral Load?
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The amount of HIV in the blood plasma
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What is a shift to the left?
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Having high levels of immsyutr neutrophils called bands in an acute bacterial infection.
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Complement system major functions:
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enhanced phagocytosis, increased vascular permeabilty, chemotaxis, cellular lysis
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Early s and sx of HIV
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Generally asymptomatic
Fatigue, headache, low-grade fever, and night sweats, usually mistaken for the flu |
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Transmission of HIV
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blood, semen, vaginal secretion, and breast milk (body fluids only)
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Normal CD4+ T Helper Cells Count
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800-1200
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Immune problems happen with CD4+ T Helper Cells Count
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below 500
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AIDS CD4+ T Helper Cells Count
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below 200
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Intermediate Chronic Clinical Manifestations of HIV
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CD4+ T Helper Cells Count of 200-500, viral load increases, HIV becomes for active
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Intermediate Chronic symptoms
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Thrush, Oral Hairy Leukoplakia, Shingles, Persistent vaginal candidal infections, Herpes, Bacterial infections, kaposi sarcoma
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Oral Hairy Leukoplakia
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is a part of the Intermediate Chronic Stage of HIV
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Kaposi Sarcoma
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Most common type of malignacy in HIV, most common in patients on immunosuppresant drugs, happens during the intermiediate chronic stage of HIV
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Late chronic or AIDS
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Innune system severly compromised,CD4+ T Helper Cells Count less than 200, rsik for oppertunistic disease, possible malignancies, wasting and dementia
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Common Oppertunisitic diseases
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Pheumocystis jiroveci pnemonia, Cryptococcal meningitis, Cytomegalovirus retinitis, Myobacterium avium complex, Kaposi Carcoma, Influenza
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Protease inhibitors
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Interfere with activity of enzyme protease in managment of HIV
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Fusion Inhibitors
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Interfere with HIV CD4 receptor site binding and entery into cells in managment of HIV
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Combination antiretroviral therapy
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Three or more drus from different groups are prescribed at full strength
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HIV Risk Factors
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Blood Transfusions before 1985, Sharded needles, sexual history, has any STDs
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Antietroviral Therapy/adherence
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Is complex, has interactions, does not work for everyone, is expensive, treament is recommened when immune suppression is great to prevent burnout
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Hemoglobin Lab Values
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Male: 13-18g/100mL
Female: 12-16 g/100mL |
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Hematocrit
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Male: 45-52%
Female: 37-48% |
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Leukocyte (WBC) Count
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4.3-10.8
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Erythrocyte (RBC) Count
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4.2-5.9
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Platelet Count
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150,000-350,000
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Thrombocytopenia
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Low Platelet count
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Hematopoiesis
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Blood Cell Production
occurs in bone marrow |
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Plasma/Blood %
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Plasma 55%/Blood 45%
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Iron Deficiency Anemia Etiology
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Inadequate dietary intake, 5-10% of ingested iron is absorbed, Malabsorption, Blood loss, Hemolysis
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Iron Deficiency Anemia Signs and Symptoms
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Pallor, Glossitis (inflammation of the tounge), Cheilitis (Inflammation fo the lips)
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Pallor
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Low Hemaglobin, low blood flow to the skin
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Treatment of iron Deficiency Anemia
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Increase intake of iron with oj on an empty stomach, liquid iron through a straw d/t teeth staining, nutritional therapy, oral or parenteral iron supplements, transfusion of packed RBCs, black stools
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Parenteral Iron Supplements
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Can be used IM or IV, IM may stain skin, always change needle before giving to prevent stain,
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At Risk groop for Iron Deficiency Anemia
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Premenopausal women, pregnant, low socioeconimic backgrounds, older adults, and individuals experiencing blood loss
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Pernicious Anemia
Cobalamin Deficiency B12 Etiology |
GI surgery, Chronic diseases of the GI tract, Long-term users of H2-histamine receptor blockers (ranidatine), alchoholism, Absence of Intrinsic Factor
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Pernicious Anemia
Cobalamin Deficiency Clinical Manifestations |
Sore (beefy) tounge, anorexia, nausea, vomitting, abdominal pain, neuromuscular manifestations- weakness, Paresthesia of the feet and hands, Ataxia (diff. walking), impaired thought process, parasthesis f the feet and hands
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Intrinsic Factor
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Protein secreted by the parietal cells of the gastric mucosa. It is required for cobalamin absorption in the small intestine
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Pernicious Anemia
Cobalamin Deficiency Causes |
Pernicious Anemia, Gastrectomy, Nutritional deficiencies, chronic alcoholism, hereditary enzymatic defects
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Pernicious Anemia
Cobalamin Deficiency B12 Treatment |
Parenteral or intranasal administration of cobalamin, increase in dietary cobalamin does not correct the anemia, still needs adequate dietary intake
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Pernicious Anemia
Cobalamin Deficiency B12 Managment |
Ensure no injuries r/t pt's diminished sensation to heat and pain, frequently evaluate patient for gastric carcinoma,
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Anemia of Chronic Disease
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Underproducation of RBC's, mild shortening of RBC servival
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Anemia of Chronic Disease Causes
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End-stage renal disease: primary factor decreased erythropoietin, chronic liver disease, chronic inflammation, malignant tumors, chronic endocrine diseases
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Anemia of Chronic Disease findings and treatment
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Increased Serum Ferritin and iron stores. Normal folate and cobalamin levels, treating underlying cause is best, rarely blood transfusions, erythropoietin therapy
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Aplastic Anemia Etiology
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Pancytopenia= decrease in all blood cell types
Low incidence Affecting 2 of every 1 million people Congential:Chromasomal alterations or Acquired: results from exposer to ionizing, radiation, chemical agents, viral and bacterial infections |
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Aplastic Anemia Manifestations
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abrupt or gradual development, symptoms caused by suppression of any or all bone marrow elements, Fatigue, dyspnea, Cardiovascular and cerebral response, neutropenia
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Aplastic Anemia Managment adn complications
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Must monitor for fever!
Preventing complications from infection and hemorrhage, untreated prognosis is poor (70% Fatal) |
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Aplastic Anemia Treatment
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Hematopoietic stem cell transplantation (HSCT)
Immunosuppressive therapy |
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Hemolytic Anemia
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Destruction or hemolysis of RBC's at a rate that exceeds production, extrinsic (aquired) more common then instrinsic
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Hemolytic Anemia manifestations
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Jaundice, dystroyed RBC's cause increased bilirubin, enlarged spleen and liver, Tubular necrosis ( hemoglobin molecules can obstruct renal tubulars)
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3 extrinsic categories
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1 physical factors
2 immune reactions 3 infectious agents and toxins |
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Who is considered at risk fr HIV?
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The CDC recommends testing for everyone between the ages of 13-64
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Considerations for diabetic patients and those taking immunosuppressives..
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at risk for infection
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A patient has a postive EIA test, what is the next step?
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Repeat the EIA and confirm the diagnosis with a western blot
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Complications of anemia
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if heart is overworked thying to get oxygen to the blood this can lead to heart failure, and heart magaely
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Anemia where this is no cell production and they are more at risk for infection
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Aplastic Anemia
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Acquired hemolytic anemia
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Physical factors: extreme force on cells
Immune reactions: antigen-antibody reactions destroy RBC's, isoimmune reactions, autoimmune reactions |
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Lymphomas
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malignant neoplasms originating in the bone marrow and lymphatic stuctures resulting in proliferation of lymphocytes
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5th most common type of cancer
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Lymphomas
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Reed-Sternberg Cells
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abnormal, giant, multi-nucteated cells located in lymph nodes, found in Hodgkins Lymphomas
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Megaloblastic Anemia
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Folic ascid deficient, similar manifestations to B-12 deficient anemia
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Hodgkin's Lymphoma S and Sx
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, weight loss, fatigue, weakness, fever chills tachycardia, night sweats,
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Hodgkins Lymphoma Clinical manifestations
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Reed-Sternberg Cells present in biopsy of lymph, 2 centameters or larger lymph nodes in cervical, axillary or inguinal lymph nodes
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