NUR 202 Module D Exam Questions
and Answers
Neutrophils - ANSWER--PHAGOCYTIZE bacteria, other foreign material, and
damaged cells.
-Short life span (12-18 hours) so a lot are produced daily
-ANC is used to determine a client's risk of infection
-ANC stands for ABSOLUTE NEUTROPHIL COUNT.
-Expected range is 1.5-8. This number tells us the # of mature circulating neutrophils
and how well the pt can fight infection.
-**THE higher the number the decreased risk of infection.
Macrophages: - ANSWER-Phagocytosis, secretes cytokines for immune system
control, aid in stimulating immediate inflammation response and AMI and CMI
functions.
Basophils - ANSWER-release histamine and heparin into blood vessels and cause
signs and symptoms of inflammation
Eosinophils: - ANSWER-LIMITS the inflammatory response so levels are high during
an allergic response.
Inflammation does not always mean...... - ANSWER-an infection is present.
-Infection is usually accompanied by inflammation. However, inflammation can occur
without invasion of organisms
Anti-body mediated immunity: - ANSWER-B cells- Memory cells, when they come
into contact with antigen it produces antibodies against that antigen.
-AMI uses antigen-antibody interactions to destroy foreign proteins.
-Primary immune response is evident 4-8 days after initial exposure to antigen.
Antibody classification: Chart 17-3 pg 298 - ANSWER--IgA: "secretory" Breast milk,
saliva, GI, respiratory, and GU tract. Very low circulating amounts.
-IgG: Plasma, interstitial fluid, it does cross the placenta and provides newborn with
passive immunity. IgG provides long-term immunity against invading organisms.
Activates macrophage and neutrophil action.
How do you acquire antibody-mediated immunity> - ANSWER--Natural active
-Artificial Active
-Natural passive
-Active passive
,natural active immunity - ANSWER-pathogens enter body and cause illness;
antibodies form in host. MOST EFFECTIVE; Longest lasting.
artifical active immunity - ANSWER-vaccinations. May need boosters b/c vaccine is
not as effective as it once was.
natural passive immunity - ANSWER-acquired by a child through placenta and
breast milk.
IgG
artificial passive immunity - ANSWER-immunity which results from the administration
of antibodies from another animal against a dangerous pathogen.
_Tetanus toxoid, or snake anti-venom.
Cell-mediated immunity - ANSWER-Think T-cells
-Immune responses initiated through specific antigen recognition by T-cells.
-Most effective against viruses.
-Several types:
-T-lymphocytes
-Macrophages
-Natural killer cells
Helper/Inducer T-Cells (CD4+) - ANSWER-Secretes cytokines
Easily recognizes self cells versus non-self cells
Suppressor T cells T8+ - ANSWER-Important in preventing the formation of
antibodies directed against normal self cells.
natural killer cells (CD16+) - ANSWER-Seek and destroys non self-cells or abnormal
self cells.
A type of white blood cell that can kill tumor cells and virus-infected cells
Cell mediated immunity is regulated by: - ANSWER-Cytokines.
They act as messengers among cell types.
Cytokines - ANSWER--Currently have 100 different cytokines
-Have a beneficial role in hematopoiesis and immune function.
-Can have detrimental effects if they are too numerous and they must be regulated.
If not they can cause: Chronic inflammation, Autoimmune diseases, or sepsis.
Erythopoietin - ANSWER-cytokine that stimulates the production of red blood cells
Interleukin-1 (IL-1) - ANSWER-causes fever
Interleukin-2 - ANSWER-Enhances natural killer cell activity against cancer cells
, Hyperacute graft rejection - ANSWER--Begins immediately upon transplantation.
Within minutes to hours.
-It is an anti-body mediated response
-Removal is required.
-Most common with Kidney transplants.
-Multiple pregnancies and multiple blood transfusions put you at risk for this.
Acute graft rejection - ANSWER--occurs within 1 week to 3 months after transplant.
-Must increase meds.
Chronic rejection - ANSWER--This type of reaction is long-standing and occurs
continuously.
-No clear cause
-Need to increase meds.
-
Best way to prevent graft rejections?> - ANSWER-HLA must match as closely as
possible.
Patients that receive a transplant will be on anti-rejection meds for how long?> > -
ANSWER-LIFE
Maintenance treatment of transplant rejection: - ANSWER-Corticosteroids
Calcineurin inhibitors
Antiproliferatives
Corticosteroids for transplant rejection - ANSWER-Corticosteroids: Broadly inhibit
cytokine production in most leukocytes, resulting in generalized immunosuppression.
**When someone is on corticosteroids, it is important to teach them to avoid crowds,
sick people, and to get their vaccines along with cancer screenings.
-Prednisone or Prednisolone.
-May cause: HTN, Hyperlipidemia, Osteoporosis, WT gain, Cushingoid appearance,
opportunistic infections, glaucoma, GI ulcer formation, hyperglycemia. Flushing and
fluid retention.
Calcineurin inhibitors - ANSWER-The inhibition of calcineurin inhibitors stops the
production and secretion of IL-2 which then prevents the activation of lymphocytes
involved in transplant rejection.
-Cyclosporine: Nephrotoxic, HTN, Tremor, CAD, Hirsutism, Gingival hyperplasia,
Opportunistic infections, malignancies, hyperuricemia, hepatotoxicity.
-Tacrolimus: Nephrotoxic, HTN, Hyperkalemia, Hypomagnesmia, Hyperglycemia,
Opportunistic infection, malignancies.
Antiproliferatives: - ANSWER-* The main action of all anti-proliferatives is to inhibit
something essential to DNA synthesis, which prevents cell division in activated
lymphocytes. Some have additional immune suppressive actions.
and Answers
Neutrophils - ANSWER--PHAGOCYTIZE bacteria, other foreign material, and
damaged cells.
-Short life span (12-18 hours) so a lot are produced daily
-ANC is used to determine a client's risk of infection
-ANC stands for ABSOLUTE NEUTROPHIL COUNT.
-Expected range is 1.5-8. This number tells us the # of mature circulating neutrophils
and how well the pt can fight infection.
-**THE higher the number the decreased risk of infection.
Macrophages: - ANSWER-Phagocytosis, secretes cytokines for immune system
control, aid in stimulating immediate inflammation response and AMI and CMI
functions.
Basophils - ANSWER-release histamine and heparin into blood vessels and cause
signs and symptoms of inflammation
Eosinophils: - ANSWER-LIMITS the inflammatory response so levels are high during
an allergic response.
Inflammation does not always mean...... - ANSWER-an infection is present.
-Infection is usually accompanied by inflammation. However, inflammation can occur
without invasion of organisms
Anti-body mediated immunity: - ANSWER-B cells- Memory cells, when they come
into contact with antigen it produces antibodies against that antigen.
-AMI uses antigen-antibody interactions to destroy foreign proteins.
-Primary immune response is evident 4-8 days after initial exposure to antigen.
Antibody classification: Chart 17-3 pg 298 - ANSWER--IgA: "secretory" Breast milk,
saliva, GI, respiratory, and GU tract. Very low circulating amounts.
-IgG: Plasma, interstitial fluid, it does cross the placenta and provides newborn with
passive immunity. IgG provides long-term immunity against invading organisms.
Activates macrophage and neutrophil action.
How do you acquire antibody-mediated immunity> - ANSWER--Natural active
-Artificial Active
-Natural passive
-Active passive
,natural active immunity - ANSWER-pathogens enter body and cause illness;
antibodies form in host. MOST EFFECTIVE; Longest lasting.
artifical active immunity - ANSWER-vaccinations. May need boosters b/c vaccine is
not as effective as it once was.
natural passive immunity - ANSWER-acquired by a child through placenta and
breast milk.
IgG
artificial passive immunity - ANSWER-immunity which results from the administration
of antibodies from another animal against a dangerous pathogen.
_Tetanus toxoid, or snake anti-venom.
Cell-mediated immunity - ANSWER-Think T-cells
-Immune responses initiated through specific antigen recognition by T-cells.
-Most effective against viruses.
-Several types:
-T-lymphocytes
-Macrophages
-Natural killer cells
Helper/Inducer T-Cells (CD4+) - ANSWER-Secretes cytokines
Easily recognizes self cells versus non-self cells
Suppressor T cells T8+ - ANSWER-Important in preventing the formation of
antibodies directed against normal self cells.
natural killer cells (CD16+) - ANSWER-Seek and destroys non self-cells or abnormal
self cells.
A type of white blood cell that can kill tumor cells and virus-infected cells
Cell mediated immunity is regulated by: - ANSWER-Cytokines.
They act as messengers among cell types.
Cytokines - ANSWER--Currently have 100 different cytokines
-Have a beneficial role in hematopoiesis and immune function.
-Can have detrimental effects if they are too numerous and they must be regulated.
If not they can cause: Chronic inflammation, Autoimmune diseases, or sepsis.
Erythopoietin - ANSWER-cytokine that stimulates the production of red blood cells
Interleukin-1 (IL-1) - ANSWER-causes fever
Interleukin-2 - ANSWER-Enhances natural killer cell activity against cancer cells
, Hyperacute graft rejection - ANSWER--Begins immediately upon transplantation.
Within minutes to hours.
-It is an anti-body mediated response
-Removal is required.
-Most common with Kidney transplants.
-Multiple pregnancies and multiple blood transfusions put you at risk for this.
Acute graft rejection - ANSWER--occurs within 1 week to 3 months after transplant.
-Must increase meds.
Chronic rejection - ANSWER--This type of reaction is long-standing and occurs
continuously.
-No clear cause
-Need to increase meds.
-
Best way to prevent graft rejections?> - ANSWER-HLA must match as closely as
possible.
Patients that receive a transplant will be on anti-rejection meds for how long?> > -
ANSWER-LIFE
Maintenance treatment of transplant rejection: - ANSWER-Corticosteroids
Calcineurin inhibitors
Antiproliferatives
Corticosteroids for transplant rejection - ANSWER-Corticosteroids: Broadly inhibit
cytokine production in most leukocytes, resulting in generalized immunosuppression.
**When someone is on corticosteroids, it is important to teach them to avoid crowds,
sick people, and to get their vaccines along with cancer screenings.
-Prednisone or Prednisolone.
-May cause: HTN, Hyperlipidemia, Osteoporosis, WT gain, Cushingoid appearance,
opportunistic infections, glaucoma, GI ulcer formation, hyperglycemia. Flushing and
fluid retention.
Calcineurin inhibitors - ANSWER-The inhibition of calcineurin inhibitors stops the
production and secretion of IL-2 which then prevents the activation of lymphocytes
involved in transplant rejection.
-Cyclosporine: Nephrotoxic, HTN, Tremor, CAD, Hirsutism, Gingival hyperplasia,
Opportunistic infections, malignancies, hyperuricemia, hepatotoxicity.
-Tacrolimus: Nephrotoxic, HTN, Hyperkalemia, Hypomagnesmia, Hyperglycemia,
Opportunistic infection, malignancies.
Antiproliferatives: - ANSWER-* The main action of all anti-proliferatives is to inhibit
something essential to DNA synthesis, which prevents cell division in activated
lymphocytes. Some have additional immune suppressive actions.
