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OCN-Oncologic Emergencies Exam 2025 Questions and Answers 100% Pass

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OCN-Oncologic Emergencies Exam 2025 Questions and Answers 100% Pass Type I hypersensitivity reaction - -Anaphylactic (immediate) -Requires previous exposure to the antigen -Can lead to death -Mediated by IgE (remember epi) > which induces the release of histamine from mast cells & basophils -Examples: allergy to peanuts, bee sting, shell fish Type II hypersensitivity reaction - -Cytotoxic response (healthy cells die as they respond to the antigens. This can cause long-term damage to cells and tissues) -Antibody attacks the antigen leading to lysis -IgG & IgM are the principal antibodies involved -Examples: hemolytic anemia, thrombocytopenia, autoimmune neutropenia. meds: Penicillin, thiazides, cephalosporin Type III hypersensitivity reaction - -Immune complex response (antigens and antibodies form complexes in the skin, blood vessels, joints, and kidney tissues. These complexes cause a series of reactions that lead to tissue damage.) -Occurs when an accumulation of antibody-antigen complexes have not been cleared 2COPYRIGHT © 2025 BY SOPHIA BENNETT, ALL RIGHTS RESERVED -This inflammatory state attracts neutrophils -Lysosomal enzymes released by neutrophils leads to tissue destruction -IgG & IgM are the principal antibodies involved -Examples: Rheumatoid arthritis (grandma), systemic lupus erythematosus, serum sickness Type IV hypersensitivity reaction - -Delayed hypersensitivity reactions, may take one to three days (or even weeks) to develop response -does not involve immunoglobulins but mediated by T cells and macrophages -Ex: transplant rejection, positive tuberculin test, contact dermatitis. treatment for Type I hypersensitivity reaction - -establish patent airway -O2 -epi -albuterol for bronchospasm -IV fluids for hypotension -diphenhydramine -methylprednisolone if no response to other drugs treatment for Type II-IV hypersensitivity reactions with chemo - -antihistamines like diphenhydramine -steroids before admin -slowing infusion rate -utilizing desensitization methods 3COPYRIGHT © 2025 BY SOPHIA BENNETT, ALL RIGHTS RESERVED Disseminated Intravascular Coagulation (DIC) - a serious disorder in which the proteins that control blood clotting become overactive. -clotting can be triggered in response to infection, cancer, or other disturbance in body. No control over the clotting system, which can lead to organ failure -the fibrinolysis system is activated, but cannot function adequately against the amount of clotting that takes place, causing bleeding symptoms of DIC - -Bleeding from venipuncture sites -Purpura, petechiae, and hematomas -Symmetric cyanosis of the fingers and toes -SOB from clots in lungs -signs of hemorrhage lab findings for DIC - increase in the D-dimer assay and Fibrin degradation products (FDP) titers decrease in plts, fibrinogen, antithrombin II, and plasminogen levels treatment for DIC - treat underlying cause and stabilize pt! -blood loss: IVF and blood products, O2, coagulation factors -clotting: clotting can be prevented with heparin, but careful monitoring of bleeding is vital. PTT tests need to be monitored to ensure heparin is functioning appropriately. antithrombin can be given too What is SIADH? - high antidiuretic hormone (ADH) production leads to water retention increased total body water -> dilutional hyponatremia 4COPYRIGHT © 2025 BY SOPHIA BENNETT, ALL RIGHTS RESERVED ADH - normally secreted from posterior pituitary gland, can come from tissue elsewhere in the body. functions to cause water to be reabsorbed instead of excreted through the kidneys SIADH treatment - -Fluid restriction -IV hypertonic saline -conivaptan/tolvaptan, demeclocycline symptoms of SIADH - -Fluid retention/overload -HTN, tachycardia -brain edema, changes in LOC -weight gain -hyponatremia -> seizure precautions septic shock - a systemic response to overwhelming infection. endotoxin (a toxin that is present inside a bacterial cell and is released whe

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Publié le
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Écrit en
2024/2025
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OCN-Oncologic Emergencies Exam
2025 Questions and Answers 100%
Pass

Type I hypersensitivity reaction - ✔✔-Anaphylactic (immediate)

-Requires previous exposure to the antigen

-Can lead to death

-Mediated by IgE (remember epi) > which induces the release of histamine from mast
cells & basophils

-Examples: allergy to peanuts, bee sting, shell fish

Type II hypersensitivity reaction - ✔✔-Cytotoxic response (healthy cells die as they
respond to the antigens. This can cause long-term damage to cells and tissues)

-Antibody attacks the antigen leading to lysis

-IgG & IgM are the principal antibodies involved

-Examples: hemolytic anemia, thrombocytopenia, autoimmune neutropenia. meds:
Penicillin, thiazides, cephalosporin

Type III hypersensitivity reaction - ✔✔-Immune complex response (antigens and
antibodies form complexes in the skin, blood vessels, joints, and kidney tissues. These
complexes cause a series of reactions that lead to tissue damage.)

-Occurs when an accumulation of antibody-antigen complexes have not been cleared


COPYRIGHT © 2025 BY SOPHIA BENNETT, ALL RIGHTS RESERVED 1

, -This inflammatory state attracts neutrophils

-Lysosomal enzymes released by neutrophils leads to tissue destruction

-IgG & IgM are the principal antibodies involved

-Examples: Rheumatoid arthritis (grandma), systemic lupus erythematosus, serum
sickness

Type IV hypersensitivity reaction - ✔✔-Delayed hypersensitivity reactions, may take
one to three days (or even weeks) to develop response

-does not involve immunoglobulins but mediated by T cells and macrophages




-Ex: transplant rejection, positive tuberculin test, contact dermatitis.

treatment for Type I hypersensitivity reaction - ✔✔-establish patent airway

-O2

-epi

-albuterol for bronchospasm

-IV fluids for hypotension

-diphenhydramine

-methylprednisolone if no response to other drugs

treatment for Type II-IV hypersensitivity reactions with chemo - ✔✔-antihistamines like
diphenhydramine

-steroids before admin

-slowing infusion rate

-utilizing desensitization methods



COPYRIGHT © 2025 BY SOPHIA BENNETT, ALL RIGHTS RESERVED 2
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