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APHON Overview Exam Studyguide

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  • December 1, 2023
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  • 2023/2024
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APHON Overview Exam Studyguide


biotherapy - ANSWER modality of tx: agents that resemble body's own defense
and surveillance systems. can augment/modulate/restore host's immune
response, direct antitumor activity, other biological effects. side effects typically
hypersensitivity rx

immune surveillance - ANSWER tumor cells express abnormal tumor antigens
on surface that can be recognized/destroyed by immune system

natural killer cells - ANSWER lymphocyte that recognizes/kills malignant cells

cytotoxic t cells - ANSWER recognize tumor-assosiated antigens and kills cells

interferons - ANSWER multiple moa's & produced w/ recombinant dna.

protein capable of protecting other cells from viral infections by interfering w/
viral replication.

family of glycoproteins include: antiviral, antiproliferative, potent
immunomodulatory effects

cytokines - ANSWER products of immune cells to enhance cytotoxic activity of
cells and increase immune response

alpha-interferon - ANSWER leukocyte-derived. tx: hairy cell leukemia,
melanoma, chronic myeloid leukemia, follicular lymphoma, multiple myeloma,
cutaneous t-cell lymphoma

beta-interferon - ANSWER fibroblast-derived. tx MS

gamma-interferon - ANSWER t-lymphocyte derived. tx chronic granulomatus
disease

interleukin-2 - ANSWER produced by t-helper cells & stimulate
growth/maturation of t-cell subsets, cytotoxic t-cells, production of lymphokines &
cytokines.

act as chemical signals b/w wbc's (revs up immune system)

retinoids - ANSWER immunomodulators that facilitate differentiation &
suppress proliferation of cancer cells

all-trans retinoic acid (atra) - ANSWER tx: aml, aml m3 subtype, apl

,increase maturation of promyelocytic blasts and rapid resolution of coagulopathy
r/t tx.

isotretinoin (accutane) - ANSWER retinoid tx neuroblastoma.

have antitumor activity unknown moa. TERATOGENIC. male/female pt must
register iPledge (fetal exposure). can also affect hearing & vision

antibodies - ANSWER proteins produced by b-lymphocytes. part of humoral
immunity of adaptive system. includes immunoglobulins (igG, igA, igM, igE, igD)

murine - ANSWER mouse-derived MoAbs. pt develops human antimouse
antibodies creating high risk of hypersensitivity rx

end in -momab

Monoclonal antibodies - ANSWER very specific. directed against single
antigenic determinant on cell surface causing antibody-dependent cellular
toxicity, direct cell death, elimination of antigen/target cell that expresses the
antigen

low toxicity

-ximab - ANSWER moab combo of human & mouse antibodies

-zumab - ANSWER moab humanized, small part of mouse antibody fused w/
human antibody

-umab - ANSWER fully humanized moabs

chimeric moab - ANSWER murine variable & human constant coupled using
recombinant dna

purpose of moabs - ANSWER attach low-dose radioisotopes to image residual
disease. target chemo, radiation, biotherapy to tumor

purge autologous bone marrow of cancer cells before transplant

selectively remove t cells responsible for gvhd from marrow prior to allogenic
transplant

efficacy increased w/ chemo or radioactive substances

rituximab - ANSWER tx relapsed/refractory b-cell lymphoma, cd20+,
non-hodgkins lymphoma (w/ chop), posttransplant lymphoproliferative d/o, &
chronic gvhd

rituximab moa - ANSWER act on CD20 antigen on surface of normal/malignant

,b lymphocytes and works w/ immune system to induce b-cell lysis

radiopharmaceuticals - ANSWER moabs that have radioactive source attached
for cancer killing effect

ibritumomab tiuxetan (zevalin) - ANSWER radiopharmaceutical tx
relapse/refractory low-grade follicular or transformed b-cell non-hodgkins
lymphoma

rituximab + ibritumomab tiuxetan - ANSWER target cd20 protein on b-cells.
given prior to high dose of radiation. causes increased toxicity and severe
infusion rx

tositumomab + iodine 131 tositumomab (bexxar) - ANSWER tx cd20+ follicular
non-hodgkin's lymphoma. moa: recognizes marker and signals immune response
then radioactive source locks on to moab, delivers radiation directly to cd20
marked cells and kills lymphoma b-cells

hematopoietic growth factors - ANSWER regulate different levels of
hematopoietic cascade. aka colony stimulating factors. primarily used for
symptom management & expedited recovery from chemo-induced bone marrow
suppression

Colony Stimulating Factors - ANSWER ptns that support hematopoiesis.
decrease myelosuppression, accelerate recovery from bmt, tx infections/parasitic
diseases, help w/ pancytopenia

gcsf (filgrastim) - ANSWER stimulates neutrophil colonies to enhance
phagocytic activity and antibody-dependent killing tendency. starting dose 5
mcg/kg/day

neulasta (pegfilgrastim) - ANSWER long-acting gcsf. given 24h post chemo.
given once per chemo cycle. max dose is 6mg. kids <45kg dose is 0.1mg/kg

gm-csf (granulocyte macrophage csf; sargramostim) - ANSWER given post bmt
w/ non-hodgkins lymphoma, all, hodgkins disease. dose: 250 mcg/kg/day.
typically iv over 2h for 21 days. broader prod of neutrophil & monocyte colonies

epoetin alfa - ANSWER hormone produced naturally by kidneys in response to
decrease O2 levels. stimulates precursor cells in marrow to produce rbcs. dose
150 u/kg 3x/week

darbepoetin (aranesp) - ANSWER long-acting epoetin. given weekly. dose
0.45mcg/kg sq. titrate dosing to not get hgb >12

ESA APPRISE - ANSWER risk management system associated w/

, erythropoiesis-stimulating factors. increase risk of tumor growth/progression, cv
events, decreased survival rates when hgb >12

oprelvekin (neumega) - ANSWER thrombopoietic growth factor. stim hsc &
megakaryocyte precursurs to pvt severe thrombocytopenia. dosing: qd sc @
50mcg/kg 24h post chemo until platelets >50k

tyrosine kinase inhibitors - ANSWER interfere w/ cell comms & growth.
primarily block epidermal growth factor receptors to pvt cell proliferation, promo
apoptosis & inh antiangiogenesis

angiogenesis - ANSWER growth of new blood vessels from existing vessels.
tumor viability is dependent for growth. vascular endothelial growth factors (vegf)
cascade major factor

bevacizumab (avastin) - ANSWER vegf inhibitor. pvt angiogenesis. tx in
relapse/refractory solid tumors

vegf inhibitors - ANSWER endostatin, thalidamide. typically used in
conjunction w/ chemo. given long-term to pvt growth/metastasis. mild SE

vaccines - ANSWER substance injected to stimulate immune system to launch
response against target in vaccine

cancer vaccine - ANSWER prophylactic. given to healthy individuals (ex: HPV).
stimulate immune system to attack viruses that can cause cancer. created by
obtaining tumor cells, irradiating them & altering them so immune system
recognizes tumor cells as foreign

goal of cancer vaccine - ANSWER produce potent immune response involving
cellular & humoral arms of immune system leading to t-cell & antibody response

gene therapy - ANSWER replace missing/mutated genes w/ healthy genes (like
faulty tumor suppressor genes: p53).

active immunotherapy: intro cytokines/tumor antigen to elicit response from
immune system

adopitive immunotherapy: cell-transfer. pt own lymphocytes modified ex vivo to
enhance antitumor activity then put back into pt

urinalysis - ANSWER prior to admin cyclophosphamide, ifosfamide, and mtx

focusing on urine pH, spec grav, rbc presence

kidney function & gfr & creat clearance - ANSWER prior to hd mtx , cisplatin,
carboplatin, ifosfamide r/t renal toxicity

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