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60 Cards in this Set
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what is the log-kill hypothesis
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the hypothesis that the fraction of the cancer cells killed during each treatment cycle is constant. (so it takes many treatments)
assumes that response to treatments is homogenous |
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what is the goldie-coldman hypothesis?
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the hypothesis that the best strategy for treatment is to initiate therapy early with combinations of active drugs.
goal is avoidance of tumor resistance. |
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what are the local modalities of cancer treatment?
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surgery and radiation
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what are the 3 systemic modalities of cancer treatment?
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chemotherapy, immunotherapy, hormonal therapy
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what are examples of liquid tumors?
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lymphomas
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what are the stages of treatment for liquid tumors?
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1. induction chemo - get pt. into remission
2. consolidation chemo - to get rid of micrometastatic disease 3. Maintenence (usu only in ALL) - constant low dose chemo to keep this leukemia in check. |
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what are the different types of treatment for solid tumors (e.g., breast, lung)
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0. surgical intervention, radiation therapy
1. adjuvent chemo - (get rid of micrometastatic disease) 2. neoadjuvant chemotherapy - given prior to any definitive surgery (shrinks tumor first). treatment for breast mostly. some lung. 3. palliative chemotherapy - improve quality of life even though it's not curable (stop tumor from pressing on smg). |
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4 response criteria terms
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Complete Response (CR) - disappearance of all evidence of tumor
Partial Response (PR) - decrease of at least 50% in diameter of all measurable lesions Stable Disease (SD) - decrease of less than 50% to increase of less than 25% in diameter product of lesion Progressive Disease (PD) - increase of more than 25% in diameter product of any lesion |
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when is a pt. considered "cured"?
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5 years after initial diagnosis without evidence of disease
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what is the definition of complete response (CR)?
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Complete Response (CR) - disappearance of all evidence of tumor
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what is the definition of partial response (PR)?
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Partial Response (PR) - decrease of at least 50% in diameter of all measurable lesions
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what is the definition of stable disease (SD)?
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Stable Disease (SD) - decrease of less than 50% to increase of less than 25% in diameter product of lesion
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what is the definition of progressive disease (PD)?
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Progressive Disease (PD) - increase of more than 25% in diameter product of any lesion
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what are the characteristics of Stage IV cancer?
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Stage IV means spread through the body. Metastatic.
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what is characteristic of stage I cancer?
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Stage I is local (no movement, no lymph nodes invaded).
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when do pts feel worst in chemo?
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7-10 days out of chemo is when they feel the worst.
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how do you treat anticipatory n/v?
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benzos
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3 types of chemo n/v?
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anticipatory (pavlovian)
acute first 24 h (peaks 4-6 h after) delayed (3-4 days after) |
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how do you prevent delayed n/v?
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take antiemetics 3-5 days after
serotonin antagonist + dexamethasone + nk1 antagonist |
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nk-1 antagonists
indications accompany.... |
approved for the treatment of both acute and delayed n/v.
MOA: blocks substance P accompany cisplatin treatment regimens |
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serotonin antagonists
2 examples, MOA, who gets these? |
e.g., Zofran, aloxi (shot w/long half-life)
blocks serotonin at 5HT3. in exam world, everyone's going to get a serotonin antagonist for prophlaxis. |
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2 serotonin antagonist adverse effects?
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H/A, hiccups
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describe dexamethasone
who gets this? |
a cortacosteroid that increases the efficacy of other antiemetics by a factor of 10(!)
good for anyone getting chemo |
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describe and name 2 dopamine antagonist antiemetics
use? |
reglan and compazine
block D2 extrapyramidal side effects in young men and old ladies good PRNs for N/V |
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PRN antiemetics?
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D2 antagonists (reglan, compazine)
benzos |
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when does your risk for infection really increase?
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when your ANC is less than 1000.
absolute neutrophil count (ANC = WBC (% bands + % neutrophils)/ 100) |
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what do myeloid growth factors do?
what's an example of a myeloid growth factor? when is it used? |
Enhance proliferation and differentiation of myeloid cell lines (**neutrophils**)
EXPENSIVE Filgrastim primary prophylaxis for chemo that we know will drain neutrophil counts. |
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when do you give filgrastim?
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after chemo is done.
(so the cells don't get killed) |
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what's the name of the myeloid growth factor that's a one-time shot?
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neulasta
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side effects of myeloid growth factors
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bone pain (actually a good sign)
fever increase in uric acid |
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if febrile and neutropenic, what should we be giving patients?
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antibiotics
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how do you calculate an ANC?
how do you interpret the results? |
WBC x (% neutrophils + % bands) /100 = ANC
ANC less than 1000 is bad, bad news for infections. |
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2 broad categories of chemotherapy
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cell-cycle specific
cell-cycle non-specific |
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drugs that affect cells that are in undergoing synthesis
describe MOA |
antimetabolites (methotrexate, e.g.)
inhibits DNA synth, normal cellular metabolism, etc. |
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describe vinca alkyloids and taxanes
describe MOA briefly major side effect? |
cell cycle specific drugs,
work best when cells are in mitosis, work just okay other times. work on mitotic tubules side effect? neurotoxicity |
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cell-cycle non-specific drug categories (the ant)
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alkylators
platinums anthracyclines |
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conventional chemotherapy classes
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1. M phase agents (vinca alkaloids and taxanes)
2. S-phase agents - antimetabolites like methotrexate 3. non-cell-cycle-specific agents (alkylators, platinums, anthracyclines) |
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prototype alkylating agent?
MOA? activated by... |
cyclophosphamide
they cause inter- and intra-strand crosslinks in DNA. DNA is alkylated, causing damage. can't unwind now. activated by enzyme in liver, so you need someone with normal liver function. also seen in rheumatology and nephrology |
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what especially serious side effect is related to cyclophosphamide?
how do you treat it? |
hemmorhagic cystitis.
acrolein metabolite "likes" bladder epithelium, can attack and cause bleeding. can treat this with mesna - binds acrolein in the bladder. also can just push fluids - pee out the acrolein. |
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what are the side effects associated with cyclophosphamide?
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hemmorhagic cystitis
immunosuppression neutropenia cardiotoxicity delayed n/v |
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prototype platinum analogue?
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cisplatin
also works by wreaking cross link havoc in DNA excreted by kidneys (>90%). always think kidneys, kidneys, kidneys. |
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cisplatin: major side effects?
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nephrotoxicity
check serum creatinine hydration also important. avoid other nephrotoxic drugs. (e.g., IV contrast) horrible, horrible n/v. used to admit people and knock them out to give them course. |
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3 antimetabolites to know
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methotrexate
5-fluorouracil cytarbine |
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methotrexate MOA
+ 4 important features (incl clearance?) |
inhibits dihydrofolate reductase
distributes into third space fluids, likes water. forms a depot of drug. may be given intrathecally renal, renal, renal clearance the one chemo drug where you monitor levels |
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what is the rescue drug for methotrexate?
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leukovorin
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describe 5FU
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antimetabolite (S phase specific)
inhibits thymidylate synthesis binds TS so it can't do its job. additive effects: leucovorin combines well with this, double covers TS nice drug because you can give it to pts with hepatic or renal dysfunction side 3: side effects? |
mucousitis
diarrhea photosensitivity |
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describe cytarabine
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antimetabolite (s phase)
can be given intrathecally leukemias, lymphomas side 3: side effects? |
myelosuppression
high dose: cerebellar toxicity (balance, foot drop) chemical conjunctivitis (use artificial tears) |
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describe vinca alkyloids
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antimicrotubules
these agents disrupt microtubule formation, induce metaphase arrest biliary clearance side 3: side effects? |
peripheral neuropathies (tingling in fingers and toes)
decreased autonomic function (constipation) CNS toxicity (vincristine) vesicants! |
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describe taxanes
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antimicrotubules
paclitaxel and docetaxel from tree bark. lots of hypersens. rxs side 3: side effects? |
peripheral neuropathy - cumulative
stomatitis hypersensitivity reactions cardiac (arrhythmias with paclitaxel) fluid retention |
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what's the prototype anthracycline?
MOA? |
cell-cycle non-specific
doxorubicin (Adriamycin)* reddish tint in bag. intercalate DNA (torsional stress) side 3: side effects? |
cardiotoxicity - idiosyncratic.
chronic: CHF type picture |
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Toperisomerase I inhibitors
prototype? |
creates multiple breaks along DNA, doesn't allow DNA to reglue.
Irinotecan - very important in treatment of colorectal cancer watch for hepatic toxicity side 3: 2 side effects |
myelosuppression
diarrhea - acute and delayed treat acute with atropine treat delayed diarrhea with immodium (can be deadly) |
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chimeric antibodies
suffix? |
most of the antibody is human, small areas are mousy. this results in less reactivity.
-ximab |
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humanized antibodies
suffix? |
almost entirely human
-zumab. |
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suffix for entirely human antibodies?
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-umab
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4 MOAs for antibody therapies
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1. apoptosis
2. complement-mediated cytotoxicity (complement cascade pokes holes in membrane) 3. antibody dependent cellular cyctotoxicity (marks for NKs) 4. radiolabeled antibodies (for lymphomas). antibody kills cells and radiates surrounding cells. |
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EGFR inhibitor side effects?
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Epidermal Growth Factor receptor inhibitor
Acneiform rash GI disturbances (diarrhea) Conjunctivitis, keratitis Pulmonary toxicity (rare) |
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briefly describe VEGF inhibitors
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(vascular endothelial growth factor inhibitor)
blocks development of new growth factors. does impair wound healing can cause hypertension |
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describe signal transduction inhibitors
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targets specific kinase in specific for chronic myelogenous leukemia
(Gleevec) first in class for oral agent to treat leukemia |
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what's an omaya?
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port in the head to get chemo into CSF.
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what are 3 drugs that are esp. associated with delayed n/v?
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cisplatin,cyclophosphamide, doxorubicin
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