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66 Cards in this Set

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